[{"page":"892 - 901","issue":"7","intvolume":"      1857","year":"2016","acknowledgement":"funded by the Medical Research Council (Grant number MC_U105674180)","month":"07","type":"journal_article","_id":"1521","date_updated":"2021-01-12T06:51:21Z","title":"Structure of bacterial respiratory complex I","day":"01","publisher":"Elsevier","scopus_import":1,"publication":"Biochimica et Biophysica Acta - Bioenergetics","date_published":"2016-07-01T00:00:00Z","abstract":[{"lang":"eng","text":"Complex I (NADH:ubiquinone oxidoreductase) plays a central role in cellular energy production, coupling electron transfer between NADH and quinone to proton translocation. It is the largest protein assembly of respiratory chains and one of the most elaborate redox membrane proteins known. Bacterial enzyme is about half the size of mitochondrial and thus provides its important &quot;minimal&quot; model. Dysfunction of mitochondrial complex I is implicated in many human neurodegenerative diseases. The L-shaped complex consists of a hydrophilic arm, where electron transfer occurs, and a membrane arm, where proton translocation takes place. We have solved the crystal structures of the hydrophilic domain of complex I from Thermus thermophilus, the membrane domain from Escherichia coli and recently of the intact, entire complex I from T. thermophilus (536. kDa, 16 subunits, 9 iron-sulphur clusters, 64 transmembrane helices). The 95. Å long electron transfer pathway through the enzyme proceeds from the primary electron acceptor flavin mononucleotide through seven conserved Fe-S clusters to the unusual elongated quinone-binding site at the interface with the membrane domain. Four putative proton translocation channels are found in the membrane domain, all linked by the central flexible axis containing charged residues. The redox energy of electron transfer is coupled to proton translocation by the as yet undefined mechanism proposed to involve long-range conformational changes. This article is part of a Special Issue entitled Respiratory complex I, edited by Volker Zickermann and Ulrich Brandt."}],"language":[{"iso":"eng"}],"publist_id":"5654","department":[{"_id":"LeSa"}],"doi":"10.1016/j.bbabio.2016.01.012","volume":1857,"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","publication_status":"published","date_created":"2018-12-11T11:52:30Z","oa_version":"None","citation":{"ieee":"J. Berrisford, R. Baradaran, and L. A. Sazanov, “Structure of bacterial respiratory complex I,” <i>Biochimica et Biophysica Acta - Bioenergetics</i>, vol. 1857, no. 7. Elsevier, pp. 892–901, 2016.","ista":"Berrisford J, Baradaran R, Sazanov LA. 2016. Structure of bacterial respiratory complex I. Biochimica et Biophysica Acta - Bioenergetics. 1857(7), 892–901.","mla":"Berrisford, John, et al. “Structure of Bacterial Respiratory Complex I.” <i>Biochimica et Biophysica Acta - Bioenergetics</i>, vol. 1857, no. 7, Elsevier, 2016, pp. 892–901, doi:<a href=\"https://doi.org/10.1016/j.bbabio.2016.01.012\">10.1016/j.bbabio.2016.01.012</a>.","short":"J. Berrisford, R. Baradaran, L.A. Sazanov, Biochimica et Biophysica Acta - Bioenergetics 1857 (2016) 892–901.","ama":"Berrisford J, Baradaran R, Sazanov LA. Structure of bacterial respiratory complex I. <i>Biochimica et Biophysica Acta - Bioenergetics</i>. 2016;1857(7):892-901. doi:<a href=\"https://doi.org/10.1016/j.bbabio.2016.01.012\">10.1016/j.bbabio.2016.01.012</a>","chicago":"Berrisford, John, Rozbeh Baradaran, and Leonid A Sazanov. “Structure of Bacterial Respiratory Complex I.” <i>Biochimica et Biophysica Acta - Bioenergetics</i>. Elsevier, 2016. <a href=\"https://doi.org/10.1016/j.bbabio.2016.01.012\">https://doi.org/10.1016/j.bbabio.2016.01.012</a>.","apa":"Berrisford, J., Baradaran, R., &#38; Sazanov, L. A. (2016). Structure of bacterial respiratory complex I. <i>Biochimica et Biophysica Acta - Bioenergetics</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.bbabio.2016.01.012\">https://doi.org/10.1016/j.bbabio.2016.01.012</a>"},"author":[{"last_name":"Berrisford","first_name":"John","full_name":"Berrisford, John"},{"first_name":"Rozbeh","full_name":"Baradaran, Rozbeh","last_name":"Baradaran"},{"last_name":"Sazanov","id":"338D39FE-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-0977-7989","first_name":"Leonid A","full_name":"Sazanov, Leonid A"}],"status":"public","quality_controlled":"1"},{"intvolume":"        16","month":"01","page":"1 - 25","issue":"1","arxiv":1,"main_file_link":[{"open_access":"1","url":"http://arxiv.org/abs/1408.3918"}],"type":"journal_article","abstract":[{"text":"We classify smooth Brunnian (i.e., unknotted on both components) embeddings (S2 × S1) ⊔ S3 → ℝ6. Any Brunnian embedding (S2 × S1) ⊔ S3 → ℝ6 is isotopic to an explicitly constructed embedding fk,m,n for some integers k, m, n such that m ≡ n (mod 2). Two embeddings fk,m,n and fk′ ,m′,n′ are isotopic if and only if k = k′, m ≡ m′ (mod 2k) and n ≡ n′ (mod 2k). We use Haefliger’s classification of embeddings S3 ⊔ S3 → ℝ6 in our proof. The relation between the embeddings (S2 × S1) ⊔ S3 → ℝ6 and S3 ⊔ S3 → ℝ6 is not trivial, however. For example, we show that there exist embeddings f: (S2 ×S1) ⊔ S3 → ℝ6 and g, g′ : S3 ⊔ S3 → ℝ6 such that the componentwise embedded connected sum f # g is isotopic to f # g′ but g is not isotopic to g′.","lang":"eng"}],"language":[{"iso":"eng"}],"publist_id":"5652","department":[{"_id":"UlWa"}],"publisher":"Independent University of Moscow","scopus_import":"1","publication":"Moscow Mathematical Journal","citation":{"ieee":"S. Avvakumov, “The classification of certain linked 3-manifolds in 6-space,” <i>Moscow Mathematical Journal</i>, vol. 16, no. 1. Independent University of Moscow, pp. 1–25, 2016.","ista":"Avvakumov S. 2016. The classification of certain linked 3-manifolds in 6-space. Moscow Mathematical Journal. 16(1), 1–25.","short":"S. Avvakumov, Moscow Mathematical Journal 16 (2016) 1–25.","mla":"Avvakumov, Sergey. “The Classification of Certain Linked 3-Manifolds in 6-Space.” <i>Moscow Mathematical Journal</i>, vol. 16, no. 1, Independent University of Moscow, 2016, pp. 1–25, doi:<a href=\"https://doi.org/10.17323/1609-4514-2016-16-1-1-25\">10.17323/1609-4514-2016-16-1-1-25</a>.","ama":"Avvakumov S. The classification of certain linked 3-manifolds in 6-space. <i>Moscow Mathematical Journal</i>. 2016;16(1):1-25. doi:<a href=\"https://doi.org/10.17323/1609-4514-2016-16-1-1-25\">10.17323/1609-4514-2016-16-1-1-25</a>","apa":"Avvakumov, S. (2016). The classification of certain linked 3-manifolds in 6-space. <i>Moscow Mathematical Journal</i>. Independent University of Moscow. <a href=\"https://doi.org/10.17323/1609-4514-2016-16-1-1-25\">https://doi.org/10.17323/1609-4514-2016-16-1-1-25</a>","chicago":"Avvakumov, Sergey. “The Classification of Certain Linked 3-Manifolds in 6-Space.” <i>Moscow Mathematical Journal</i>. Independent University of Moscow, 2016. <a href=\"https://doi.org/10.17323/1609-4514-2016-16-1-1-25\">https://doi.org/10.17323/1609-4514-2016-16-1-1-25</a>."},"quality_controlled":"1","article_type":"original","publication_status":"published","acknowledgement":"I thank A. Skopenkov for telling me about the problem and for his useful remarks.  I also thank A. Sossinsky,\r\nA. Zhubr, M. Skopenkov, P. Akhmetiev, and an anonymous referee for their feedback.  Author was partially\r\nsupported by Dobrushin fellowship, 2013, and by RFBR grant 15-01-06302.","year":"2016","oa":1,"publication_identifier":{"eissn":["1609-4514"]},"title":"The classification of certain linked 3-manifolds in 6-space","article_processing_charge":"No","_id":"1522","date_updated":"2022-02-25T10:15:57Z","external_id":{"arxiv":["1408.3918"]},"day":"01","date_published":"2016-01-01T00:00:00Z","oa_version":"Preprint","status":"public","author":[{"id":"3827DAC8-F248-11E8-B48F-1D18A9856A87","last_name":"Avvakumov","first_name":"Serhii","full_name":"Avvakumov, Serhii"}],"doi":"10.17323/1609-4514-2016-16-1-1-25","volume":16,"date_created":"2018-12-11T11:52:30Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87"},{"publication":"Proceedings of the American Mathematical Society","scopus_import":1,"publisher":"American Mathematical Society","language":[{"iso":"eng"}],"publist_id":"5650","department":[{"_id":"UlWa"}],"abstract":[{"text":"For random graphs, the containment problem considers the probability that a binomial random graph G(n, p) contains a given graph as a substructure. When asking for the graph as a topological minor, i.e., for a copy of a subdivision of the given graph, it is well known that the (sharp) threshold is at p = 1/n. We consider a natural analogue of this question for higher-dimensional random complexes Xk(n, p), first studied by Cohen, Costa, Farber and Kappeler for k = 2. Improving previous results, we show that p = Θ(1/ √n) is the (coarse) threshold for containing a subdivision of any fixed complete 2-complex. For higher dimensions k &gt; 2, we get that p = O(n−1/k) is an upper bound for the threshold probability of containing a subdivision of a fixed k-dimensional complex.","lang":"eng"}],"publication_status":"published","citation":{"short":"A. Gundert, U. Wagner, Proceedings of the American Mathematical Society 144 (2016) 1815–1828.","mla":"Gundert, Anna, and Uli Wagner. “On Topological Minors in Random Simplicial Complexes.” <i>Proceedings of the American Mathematical Society</i>, vol. 144, no. 4, American Mathematical Society, 2016, pp. 1815–28, doi:<a href=\"https://doi.org/10.1090/proc/12824\">10.1090/proc/12824</a>.","ieee":"A. Gundert and U. Wagner, “On topological minors in random simplicial complexes,” <i>Proceedings of the American Mathematical Society</i>, vol. 144, no. 4. American Mathematical Society, pp. 1815–1828, 2016.","ista":"Gundert A, Wagner U. 2016. On topological minors in random simplicial complexes. Proceedings of the American Mathematical Society. 144(4), 1815–1828.","chicago":"Gundert, Anna, and Uli Wagner. “On Topological Minors in Random Simplicial Complexes.” <i>Proceedings of the American Mathematical Society</i>. American Mathematical Society, 2016. <a href=\"https://doi.org/10.1090/proc/12824\">https://doi.org/10.1090/proc/12824</a>.","apa":"Gundert, A., &#38; Wagner, U. (2016). On topological minors in random simplicial complexes. <i>Proceedings of the American Mathematical Society</i>. American Mathematical Society. <a href=\"https://doi.org/10.1090/proc/12824\">https://doi.org/10.1090/proc/12824</a>","ama":"Gundert A, Wagner U. On topological minors in random simplicial complexes. <i>Proceedings of the American Mathematical Society</i>. 2016;144(4):1815-1828. doi:<a href=\"https://doi.org/10.1090/proc/12824\">10.1090/proc/12824</a>"},"quality_controlled":"1","issue":"4","page":"1815 - 1828","month":"04","intvolume":"       144","type":"journal_article","main_file_link":[{"url":"http://arxiv.org/abs/1404.2106","open_access":"1"}],"date_published":"2016-04-01T00:00:00Z","day":"01","volume":144,"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","date_created":"2018-12-11T11:52:30Z","doi":"10.1090/proc/12824","author":[{"last_name":"Gundert","first_name":"Anna","full_name":"Gundert, Anna"},{"last_name":"Wagner","id":"36690CA2-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-1494-0568","first_name":"Uli","full_name":"Wagner, Uli"}],"status":"public","oa_version":"Preprint","oa":1,"year":"2016","acknowledgement":"This research was supported by the Swiss National Science Foundation (SNF Projects 200021-125309 and 200020-138230","_id":"1523","date_updated":"2021-01-12T06:51:22Z","title":"On topological minors in random simplicial complexes"},{"page":"173 - 191","ec_funded":1,"intvolume":"      9271","month":"01","type":"conference","main_file_link":[{"open_access":"1","url":"http://arxiv.org/abs/1501.00440"}],"publisher":"Springer","scopus_import":1,"abstract":[{"lang":"eng","text":"When designing genetic circuits, the typical primitives used in major existing modelling formalisms are gene interaction graphs, where edges between genes denote either an activation or inhibition relation. However, when designing experiments, it is important to be precise about the low-level mechanistic details as to how each such relation is implemented. The rule-based modelling language Kappa allows to unambiguously specify mechanistic details such as DNA binding sites, dimerisation of transcription factors, or co-operative interactions. Such a detailed description comes with complexity and computationally costly executions. We propose a general method for automatically transforming a rule-based program, by eliminating intermediate species and adjusting the rate constants accordingly. To the best of our knowledge, we show the first automated reduction of rule-based models based on equilibrium approximations.\r\nOur algorithm is an adaptation of an existing algorithm, which was designed for reducing reaction-based programs; our version of the algorithm scans the rule-based Kappa model in search for those interaction patterns known to be amenable to equilibrium approximations (e.g. Michaelis-Menten scheme). Additional checks are then performed in order to verify if the reduction is meaningful in the context of the full model. The reduced model is efficiently obtained by static inspection over the rule-set. The tool is tested on a detailed rule-based model of a λ-phage switch, which lists 92 rules and 13 agents. The reduced model has 11 rules and 5 agents, and provides a dramatic reduction in simulation time of several orders of magnitude."}],"language":[{"iso":"eng"}],"publist_id":"5649","department":[{"_id":"CaGu"},{"_id":"ToHe"}],"publication_status":"published","quality_controlled":"1","alternative_title":["LNCS"],"citation":{"ama":"Beica A, Guet CC, Petrov T. Efficient reduction of kappa models by static inspection of the rule-set. In: Vol 9271. Springer; 2016:173-191. doi:<a href=\"https://doi.org/10.1007/978-3-319-26916-0_10\">10.1007/978-3-319-26916-0_10</a>","chicago":"Beica, Andreea, Calin C Guet, and Tatjana Petrov. “Efficient Reduction of Kappa Models by Static Inspection of the Rule-Set,” 9271:173–91. Springer, 2016. <a href=\"https://doi.org/10.1007/978-3-319-26916-0_10\">https://doi.org/10.1007/978-3-319-26916-0_10</a>.","apa":"Beica, A., Guet, C. C., &#38; Petrov, T. (2016). Efficient reduction of kappa models by static inspection of the rule-set (Vol. 9271, pp. 173–191). Presented at the HSB: Hybrid Systems Biology, Madrid, Spain: Springer. <a href=\"https://doi.org/10.1007/978-3-319-26916-0_10\">https://doi.org/10.1007/978-3-319-26916-0_10</a>","ista":"Beica A, Guet CC, Petrov T. 2016. Efficient reduction of kappa models by static inspection of the rule-set. HSB: Hybrid Systems Biology, LNCS, vol. 9271, 173–191.","ieee":"A. Beica, C. C. Guet, and T. Petrov, “Efficient reduction of kappa models by static inspection of the rule-set,” presented at the HSB: Hybrid Systems Biology, Madrid, Spain, 2016, vol. 9271, pp. 173–191.","short":"A. Beica, C.C. Guet, T. Petrov, in:, Springer, 2016, pp. 173–191.","mla":"Beica, Andreea, et al. <i>Efficient Reduction of Kappa Models by Static Inspection of the Rule-Set</i>. Vol. 9271, Springer, 2016, pp. 173–91, doi:<a href=\"https://doi.org/10.1007/978-3-319-26916-0_10\">10.1007/978-3-319-26916-0_10</a>."},"oa":1,"project":[{"call_identifier":"FP7","grant_number":"291734","_id":"25681D80-B435-11E9-9278-68D0E5697425","name":"International IST Postdoc Fellowship Programme"}],"acknowledgement":"This research was supported by the People Programme (Marie Curie Actions) of the European Union’s Seventh Framework Programme (FP7/2007-2013) under REA grant agreement no. 291734, and the SNSF Early Postdoc.Mobility Fellowship, the grant number P2EZP2_148797.","year":"2016","date_updated":"2021-01-12T06:51:22Z","_id":"1524","conference":{"location":"Madrid, Spain","name":"HSB: Hybrid Systems Biology","start_date":"2015-09-04","end_date":"2015-09-05"},"title":"Efficient reduction of kappa models by static inspection of the rule-set","day":"10","date_published":"2016-01-10T00:00:00Z","doi":"10.1007/978-3-319-26916-0_10","date_created":"2018-12-11T11:52:31Z","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","volume":9271,"oa_version":"Preprint","status":"public","author":[{"last_name":"Beica","first_name":"Andreea","full_name":"Beica, Andreea"},{"full_name":"Guet, Calin C","first_name":"Calin C","orcid":"0000-0001-6220-2052","id":"47F8433E-F248-11E8-B48F-1D18A9856A87","last_name":"Guet"},{"full_name":"Petrov, Tatjana","first_name":"Tatjana","orcid":"0000-0002-9041-0905","id":"3D5811FC-F248-11E8-B48F-1D18A9856A87","last_name":"Petrov"}]},{"_id":"1526","date_updated":"2021-01-12T06:51:23Z","conference":{"name":"VMCAI: Verification, Model Checking and Abstract Interpretation","location":"St. Petersburg, FL, USA","end_date":"2016-01-19","start_date":"2016-01-17"},"title":"Lipschitz robustness of timed I/O systems","oa":1,"year":"2016","acknowledgement":"This research was supported in part by the European Research Council (ERC) under grant 267989 (QUAREM), by the Austrian Science Fund (FWF) under grants S11402-N23 (RiSE) and Z211-N23 (Wittgenstein Award), and by the National Science Centre (NCN), Poland under grant 2014/15/D/ST6/04543.","project":[{"name":"Quantitative Reactive Modeling","_id":"25EE3708-B435-11E9-9278-68D0E5697425","grant_number":"267989","call_identifier":"FP7"},{"grant_number":"Z211","call_identifier":"FWF","name":"The Wittgenstein Prize","_id":"25F42A32-B435-11E9-9278-68D0E5697425"},{"grant_number":"S 11407_N23","call_identifier":"FWF","name":"Rigorous Systems Engineering","_id":"25832EC2-B435-11E9-9278-68D0E5697425"}],"doi":"10.1007/978-3-662-49122-5_12","volume":9583,"date_created":"2018-12-11T11:52:32Z","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","oa_version":"Preprint","author":[{"orcid":"0000−0002−2985−7724","full_name":"Henzinger, Thomas A","first_name":"Thomas A","last_name":"Henzinger","id":"40876CD8-F248-11E8-B48F-1D18A9856A87"},{"id":"2FC5DA74-F248-11E8-B48F-1D18A9856A87","last_name":"Otop","first_name":"Jan","full_name":"Otop, Jan"},{"last_name":"Samanta","id":"3D2AAC08-F248-11E8-B48F-1D18A9856A87","full_name":"Samanta, Roopsha","first_name":"Roopsha"}],"status":"public","day":"01","date_published":"2016-01-01T00:00:00Z","type":"conference","main_file_link":[{"open_access":"1","url":"http://arxiv.org/abs/1506.01233"}],"ec_funded":1,"page":"250 - 267","intvolume":"      9583","month":"01","publication_status":"published","citation":{"ieee":"T. A. Henzinger, J. Otop, and R. Samanta, “Lipschitz robustness of timed I/O systems,” presented at the VMCAI: Verification, Model Checking and Abstract Interpretation, St. Petersburg, FL, USA, 2016, vol. 9583, pp. 250–267.","ista":"Henzinger TA, Otop J, Samanta R. 2016. Lipschitz robustness of timed I/O systems. VMCAI: Verification, Model Checking and Abstract Interpretation, LNCS, vol. 9583, 250–267.","short":"T.A. Henzinger, J. Otop, R. Samanta, in:, Springer, 2016, pp. 250–267.","mla":"Henzinger, Thomas A., et al. <i>Lipschitz Robustness of Timed I/O Systems</i>. Vol. 9583, Springer, 2016, pp. 250–67, doi:<a href=\"https://doi.org/10.1007/978-3-662-49122-5_12\">10.1007/978-3-662-49122-5_12</a>.","ama":"Henzinger TA, Otop J, Samanta R. Lipschitz robustness of timed I/O systems. In: Vol 9583. Springer; 2016:250-267. doi:<a href=\"https://doi.org/10.1007/978-3-662-49122-5_12\">10.1007/978-3-662-49122-5_12</a>","chicago":"Henzinger, Thomas A, Jan Otop, and Roopsha Samanta. “Lipschitz Robustness of Timed I/O Systems,” 9583:250–67. Springer, 2016. <a href=\"https://doi.org/10.1007/978-3-662-49122-5_12\">https://doi.org/10.1007/978-3-662-49122-5_12</a>.","apa":"Henzinger, T. A., Otop, J., &#38; Samanta, R. (2016). Lipschitz robustness of timed I/O systems (Vol. 9583, pp. 250–267). Presented at the VMCAI: Verification, Model Checking and Abstract Interpretation, St. Petersburg, FL, USA: Springer. <a href=\"https://doi.org/10.1007/978-3-662-49122-5_12\">https://doi.org/10.1007/978-3-662-49122-5_12</a>"},"quality_controlled":"1","alternative_title":["LNCS"],"publisher":"Springer","scopus_import":1,"abstract":[{"text":"We present the first study of robustness of systems that are both timed as well as reactive (I/O). We study the behavior of such timed I/O systems in the presence of uncertain inputs and formalize their robustness using the analytic notion of Lipschitz continuity: a timed I/O system is K-(Lipschitz) robust if the perturbation in its output is at most K times the perturbation in its input. We quantify input and output perturbation using similarity functions over timed words such as the timed version of the Manhattan distance and the Skorokhod distance. We consider two models of timed I/O systems — timed transducers and asynchronous sequential circuits. We show that K-robustness of timed transducers can be decided in polynomial space under certain conditions. For asynchronous sequential circuits, we reduce K-robustness w.r.t. timed Manhattan distances to K-robustness of discrete letter-to-letter transducers and show PSpace-completeness of the problem.","lang":"eng"}],"department":[{"_id":"ToHe"}],"language":[{"iso":"eng"}],"publist_id":"5647"},{"status":"public","author":[{"last_name":"Chatterjee","id":"2E5DCA20-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-4561-241X","full_name":"Chatterjee, Krishnendu","first_name":"Krishnendu"},{"last_name":"Chmelik","id":"3624234E-F248-11E8-B48F-1D18A9856A87","first_name":"Martin","full_name":"Chmelik, Martin"},{"first_name":"Raghav","full_name":"Gupta, Raghav","last_name":"Gupta"},{"last_name":"Kanodia","full_name":"Kanodia, Ayush","first_name":"Ayush"}],"oa_version":"Preprint","date_created":"2018-12-11T11:52:33Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","volume":234,"doi":"10.1016/j.artint.2016.01.007","external_id":{"arxiv":["1411.3880"]},"date_published":"2016-05-01T00:00:00Z","day":"01","title":"Optimal cost almost-sure reachability in POMDPs","article_processing_charge":"No","related_material":{"record":[{"relation":"earlier_version","status":"public","id":"1820"},{"status":"public","relation":"earlier_version","id":"5425"}]},"date_updated":"2023-02-23T12:25:49Z","_id":"1529","acknowledgement":"We thank Blai Bonet for helping us with RTDP-Bel. The research was partly supported by Austrian Science Fund (FWF) Grant No P23499-N23, FWF NFN Grant No S11407-N23 (RiSE), ERC Start grant (279307: Graph Games), and Microsoft faculty fellows award.","project":[{"_id":"2584A770-B435-11E9-9278-68D0E5697425","name":"Modern Graph Algorithmic Techniques in Formal Verification","call_identifier":"FWF","grant_number":"P 23499-N23"},{"call_identifier":"FWF","grant_number":"S 11407_N23","_id":"25832EC2-B435-11E9-9278-68D0E5697425","name":"Rigorous Systems Engineering"},{"_id":"2581B60A-B435-11E9-9278-68D0E5697425","name":"Quantitative Graph Games: Theory and Applications","call_identifier":"FP7","grant_number":"279307"}],"year":"2016","oa":1,"quality_controlled":"1","citation":{"ieee":"K. Chatterjee, M. Chmelik, R. Gupta, and A. Kanodia, “Optimal cost almost-sure reachability in POMDPs,” <i>Artificial Intelligence</i>, vol. 234. Elsevier, pp. 26–48, 2016.","ista":"Chatterjee K, Chmelik M, Gupta R, Kanodia A. 2016. Optimal cost almost-sure reachability in POMDPs. Artificial Intelligence. 234, 26–48.","short":"K. Chatterjee, M. Chmelik, R. Gupta, A. Kanodia, Artificial Intelligence 234 (2016) 26–48.","mla":"Chatterjee, Krishnendu, et al. “Optimal Cost Almost-Sure Reachability in POMDPs.” <i>Artificial Intelligence</i>, vol. 234, Elsevier, 2016, pp. 26–48, doi:<a href=\"https://doi.org/10.1016/j.artint.2016.01.007\">10.1016/j.artint.2016.01.007</a>.","ama":"Chatterjee K, Chmelik M, Gupta R, Kanodia A. Optimal cost almost-sure reachability in POMDPs. <i>Artificial Intelligence</i>. 2016;234:26-48. doi:<a href=\"https://doi.org/10.1016/j.artint.2016.01.007\">10.1016/j.artint.2016.01.007</a>","chicago":"Chatterjee, Krishnendu, Martin Chmelik, Raghav Gupta, and Ayush Kanodia. “Optimal Cost Almost-Sure Reachability in POMDPs.” <i>Artificial Intelligence</i>. Elsevier, 2016. <a href=\"https://doi.org/10.1016/j.artint.2016.01.007\">https://doi.org/10.1016/j.artint.2016.01.007</a>.","apa":"Chatterjee, K., Chmelik, M., Gupta, R., &#38; Kanodia, A. (2016). Optimal cost almost-sure reachability in POMDPs. <i>Artificial Intelligence</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.artint.2016.01.007\">https://doi.org/10.1016/j.artint.2016.01.007</a>"},"publication_status":"published","language":[{"iso":"eng"}],"publist_id":"5642","department":[{"_id":"KrCh"}],"abstract":[{"lang":"eng","text":"We consider partially observable Markov decision processes (POMDPs) with a set of target states and an integer cost associated with every transition. The optimization objective we study asks to minimize the expected total cost of reaching a state in the target set, while ensuring that the target set is reached almost surely (with probability 1). We show that for integer costs approximating the optimal cost is undecidable. For positive costs, our results are as follows: (i) we establish matching lower and upper bounds for the optimal cost, both double exponential in the POMDP state space size; (ii) we show that the problem of approximating the optimal cost is decidable and present approximation algorithms developing on the existing algorithms for POMDPs with finite-horizon objectives. While the worst-case running time of our algorithm is double exponential, we also present efficient stopping criteria for the algorithm and show experimentally that it performs well in many examples of interest."}],"scopus_import":1,"publication":"Artificial Intelligence","publisher":"Elsevier","main_file_link":[{"open_access":"1","url":"http://arxiv.org/abs/1411.3880"}],"arxiv":1,"type":"journal_article","month":"05","intvolume":"       234","page":"26 - 48","ec_funded":1},{"intvolume":"       270","month":"06","page":"4340 - 4368","ec_funded":1,"issue":"11","main_file_link":[{"open_access":"1","url":"http://arxiv.org/abs/1508.07321"}],"type":"journal_article","abstract":[{"text":"We provide general conditions for which bosonic quadratic Hamiltonians on Fock spaces can be diagonalized by Bogoliubov transformations. Our results cover the case when quantum systems have infinite degrees of freedom and the associated one-body kinetic and paring operators are unbounded. Our sufficient conditions are optimal in the sense that they become necessary when the relevant one-body operators commute.","lang":"eng"}],"language":[{"iso":"eng"}],"department":[{"_id":"RoSe"}],"publist_id":"5626","publisher":"Academic Press","scopus_import":1,"publication":"Journal of Functional Analysis","quality_controlled":"1","citation":{"apa":"Nam, P., Napiórkowski, M. M., &#38; Solovej, J. (2016). Diagonalization of bosonic quadratic Hamiltonians by Bogoliubov transformations. <i>Journal of Functional Analysis</i>. Academic Press. <a href=\"https://doi.org/10.1016/j.jfa.2015.12.007\">https://doi.org/10.1016/j.jfa.2015.12.007</a>","chicago":"Nam, Phan, Marcin M Napiórkowski, and Jan Solovej. “Diagonalization of Bosonic Quadratic Hamiltonians by Bogoliubov Transformations.” <i>Journal of Functional Analysis</i>. Academic Press, 2016. <a href=\"https://doi.org/10.1016/j.jfa.2015.12.007\">https://doi.org/10.1016/j.jfa.2015.12.007</a>.","ama":"Nam P, Napiórkowski MM, Solovej J. Diagonalization of bosonic quadratic Hamiltonians by Bogoliubov transformations. <i>Journal of Functional Analysis</i>. 2016;270(11):4340-4368. doi:<a href=\"https://doi.org/10.1016/j.jfa.2015.12.007\">10.1016/j.jfa.2015.12.007</a>","mla":"Nam, Phan, et al. “Diagonalization of Bosonic Quadratic Hamiltonians by Bogoliubov Transformations.” <i>Journal of Functional Analysis</i>, vol. 270, no. 11, Academic Press, 2016, pp. 4340–68, doi:<a href=\"https://doi.org/10.1016/j.jfa.2015.12.007\">10.1016/j.jfa.2015.12.007</a>.","short":"P. Nam, M.M. Napiórkowski, J. Solovej, Journal of Functional Analysis 270 (2016) 4340–4368.","ista":"Nam P, Napiórkowski MM, Solovej J. 2016. Diagonalization of bosonic quadratic Hamiltonians by Bogoliubov transformations. Journal of Functional Analysis. 270(11), 4340–4368.","ieee":"P. Nam, M. M. Napiórkowski, and J. Solovej, “Diagonalization of bosonic quadratic Hamiltonians by Bogoliubov transformations,” <i>Journal of Functional Analysis</i>, vol. 270, no. 11. Academic Press, pp. 4340–4368, 2016."},"publication_status":"published","year":"2016","project":[{"name":"International IST Postdoc Fellowship Programme","_id":"25681D80-B435-11E9-9278-68D0E5697425","grant_number":"291734","call_identifier":"FP7"},{"call_identifier":"FWF","grant_number":"P27533_N27","_id":"25C878CE-B435-11E9-9278-68D0E5697425","name":"Structure of the Excitation Spectrum for Many-Body Quantum Systems"}],"acknowledgement":"We thank Jan Dereziński for several inspiring discussions and useful remarks. We thank the referee for helpful comments. J.P.S. thanks the Erwin Schrödinger Institute for the hospitality during the thematic programme “Quantum many-body systems, random matrices, and disorder”. We gratefully acknowledge the financial supports by the European Union's Seventh Framework Programme under the ERC Advanced Grant ERC-2012-AdG 321029 (J.P.S.) and the REA grant agreement No. 291734 (P.T.N.), as well as the support of the National Science Center (NCN) grant No. 2012/07/N/ST1/03185 and the Austrian Science Fund (FWF) project No. P 27533-N27 (M.N.).","oa":1,"title":"Diagonalization of bosonic quadratic Hamiltonians by Bogoliubov transformations","date_updated":"2021-01-12T06:51:30Z","_id":"1545","day":"01","date_published":"2016-06-01T00:00:00Z","oa_version":"Submitted Version","author":[{"last_name":"Nam","id":"404092F4-F248-11E8-B48F-1D18A9856A87","full_name":"Nam, Phan","first_name":"Phan"},{"first_name":"Marcin M","full_name":"Napiórkowski, Marcin M","id":"4197AD04-F248-11E8-B48F-1D18A9856A87","last_name":"Napiórkowski"},{"last_name":"Solovej","first_name":"Jan","full_name":"Solovej, Jan"}],"status":"public","doi":"10.1016/j.jfa.2015.12.007","date_created":"2018-12-11T11:52:38Z","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","volume":270},{"publication_status":"published","quality_controlled":"1","citation":{"ista":"Qi Q, Toll Riera M, Heilbron K, Preston G, Maclean RC. 2016. The genomic basis of adaptation to the fitness cost of rifampicin resistance in Pseudomonas aeruginosa. Proceedings of the Royal Society of London Series B Biological Sciences. 283(1822), 20152452.","ieee":"Q. Qi, M. Toll Riera, K. Heilbron, G. Preston, and R. C. Maclean, “The genomic basis of adaptation to the fitness cost of rifampicin resistance in Pseudomonas aeruginosa,” <i>Proceedings of the Royal Society of London Series B Biological Sciences</i>, vol. 283, no. 1822. Royal Society, The, 2016.","short":"Q. Qi, M. Toll Riera, K. Heilbron, G. Preston, R.C. Maclean, Proceedings of the Royal Society of London Series B Biological Sciences 283 (2016).","mla":"Qi, Qin, et al. “The Genomic Basis of Adaptation to the Fitness Cost of Rifampicin Resistance in Pseudomonas Aeruginosa.” <i>Proceedings of the Royal Society of London Series B Biological Sciences</i>, vol. 283, no. 1822, 20152452, Royal Society, The, 2016, doi:<a href=\"https://doi.org/10.1098/rspb.2015.2452\">10.1098/rspb.2015.2452</a>.","ama":"Qi Q, Toll Riera M, Heilbron K, Preston G, Maclean RC. The genomic basis of adaptation to the fitness cost of rifampicin resistance in Pseudomonas aeruginosa. <i>Proceedings of the Royal Society of London Series B Biological Sciences</i>. 2016;283(1822). doi:<a href=\"https://doi.org/10.1098/rspb.2015.2452\">10.1098/rspb.2015.2452</a>","apa":"Qi, Q., Toll Riera, M., Heilbron, K., Preston, G., &#38; Maclean, R. C. (2016). The genomic basis of adaptation to the fitness cost of rifampicin resistance in Pseudomonas aeruginosa. <i>Proceedings of the Royal Society of London Series B Biological Sciences</i>. Royal Society, The. <a href=\"https://doi.org/10.1098/rspb.2015.2452\">https://doi.org/10.1098/rspb.2015.2452</a>","chicago":"Qi, Qin, Macarena Toll Riera, Karl Heilbron, Gail Preston, and R Craig Maclean. “The Genomic Basis of Adaptation to the Fitness Cost of Rifampicin Resistance in Pseudomonas Aeruginosa.” <i>Proceedings of the Royal Society of London Series B Biological Sciences</i>. Royal Society, The, 2016. <a href=\"https://doi.org/10.1098/rspb.2015.2452\">https://doi.org/10.1098/rspb.2015.2452</a>."},"publisher":"Royal Society, The","scopus_import":1,"publication":"Proceedings of the Royal Society of London Series B Biological Sciences","file":[{"file_id":"4899","content_type":"application/pdf","checksum":"78ffe70c1c88af3856d31ca6b7195a27","creator":"system","access_level":"open_access","file_size":626804,"date_created":"2018-12-12T10:11:43Z","file_name":"IST-2016-488-v1+1_20152452.full.pdf","date_updated":"2020-07-14T12:45:02Z","relation":"main_file"}],"file_date_updated":"2020-07-14T12:45:02Z","abstract":[{"lang":"eng","text":"Antibiotic resistance carries a fitness cost that must be overcome in order for resistance to persist over the long term. Compensatory mutations that recover the functional defects associated with resistance mutations have been argued to play a key role in overcoming the cost of resistance, but compensatory mutations are expected to be rare relative to generally beneficial mutations that increase fitness, irrespective of antibiotic resistance. Given this asymmetry, population genetics theory predicts that populations should adapt by compensatory mutations when the cost of resistance is large, whereas generally beneficial mutations should drive adaptation when the cost of resistance is small. We tested this prediction by determining the genomic mechanisms underpinning adaptation to antibiotic-free conditions in populations of the pathogenic bacterium Pseudomonas aeruginosa that carry costly antibiotic resistance mutations. Whole-genome sequencing revealed that populations founded by high-cost rifampicin-resistant mutants adapted via compensatory mutations in three genes of the RNA polymerase core enzyme, whereas populations founded by low-cost mutants adapted by generally beneficial mutations, predominantly in the quorum-sensing transcriptional regulator gene lasR. Even though the importance of compensatory evolution in maintaining resistance has been widely recognized, our study shows that the roles of general adaptation in maintaining resistance should not be underestimated and highlights the need to understand how selection at other sites in the genome influences the dynamics of resistance alleles in clinical settings."}],"language":[{"iso":"eng"}],"department":[{"_id":"ToBo"}],"publist_id":"5619","ddc":["570"],"type":"journal_article","issue":"1822","intvolume":"       283","pubrep_id":"488","article_number":"20152452","month":"01","doi":"10.1098/rspb.2015.2452","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","date_created":"2018-12-11T11:52:40Z","volume":283,"oa_version":"Published Version","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"author":[{"id":"3B22D412-F248-11E8-B48F-1D18A9856A87","last_name":"Qi","first_name":"Qin","full_name":"Qi, Qin","orcid":"0000-0002-6148-2416"},{"last_name":"Toll Riera","full_name":"Toll Riera, Macarena","first_name":"Macarena"},{"first_name":"Karl","full_name":"Heilbron, Karl","last_name":"Heilbron"},{"last_name":"Preston","first_name":"Gail","full_name":"Preston, Gail"},{"last_name":"Maclean","first_name":"R Craig","full_name":"Maclean, R Craig"}],"status":"public","day":"13","date_published":"2016-01-13T00:00:00Z","date_updated":"2021-01-12T06:51:33Z","_id":"1552","title":"The genomic basis of adaptation to the fitness cost of rifampicin resistance in Pseudomonas aeruginosa","oa":1,"year":"2016","acknowledgement":"We thank the High-Throughput Genomics Group at the Wellcome Trust Centre for Human Genetics funded by Wellcome\r\nTrust grant reference 090532/Z/09/Z and Medical Research Council Hub grant no. G0900747 91070 for generation of the high-throughput sequencing data. We thank Wook Kim and two anonymous reviewers for their constructive feedback on previous versions of our manuscript.","has_accepted_license":"1"},{"issue":"2","page":"363 - 421","month":"04","intvolume":"        29","acknowledgement":"The authors would like to thank the anonymous reviewers of this paper. We also would like to express our appreciation to the program committee and the anonymous reviewers for CRYPTO 2010. The first author thanks Sherman S. M. Chow for his comment on group signatures in Sect. 7.1.","year":"2016","type":"journal_article","_id":"1592","date_updated":"2021-01-12T06:51:49Z","title":"Structure preserving signatures and commitments to group elements","scopus_import":1,"publication":"Journal of Cryptology","date_published":"2016-04-01T00:00:00Z","day":"01","publisher":"Springer","department":[{"_id":"KrPi"}],"language":[{"iso":"eng"}],"publist_id":"5579","abstract":[{"lang":"eng","text":"A modular approach to constructing cryptographic protocols leads to simple designs but often inefficient instantiations. On the other hand, ad hoc constructions may yield efficient protocols at the cost of losing conceptual simplicity. We suggest a new design paradigm, structure-preserving cryptography, that provides a way to construct modular protocols with reasonable efficiency while retaining conceptual simplicity. A cryptographic scheme over a bilinear group is called structure-preserving if its public inputs and outputs consist of elements from the bilinear groups and their consistency can be verified by evaluating pairing-product equations. As structure-preserving schemes smoothly interoperate with each other, they are useful as building blocks in modular design of cryptographic applications. This paper introduces structure-preserving commitment and signature schemes over bilinear groups with several desirable properties. The commitment schemes include homomorphic, trapdoor and length-reducing commitments to group elements, and the structure-preserving signature schemes are the first ones that yield constant-size signatures on multiple group elements. A structure-preserving signature scheme is called automorphic if the public keys lie in the message space, which cannot be achieved by compressing inputs via a cryptographic hash function, as this would destroy the mathematical structure we are trying to preserve. Automorphic signatures can be used for building certification chains underlying privacy-preserving protocols. Among a vast number of applications of structure-preserving protocols, we present an efficient round-optimal blind-signature scheme and a group signature scheme with an efficient and concurrently secure protocol for enrolling new members."}],"volume":29,"publication_status":"published","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","date_created":"2018-12-11T11:52:54Z","doi":"10.1007/s00145-014-9196-7","citation":{"ieee":"M. Abe, G. Fuchsbauer, J. Groth, K. Haralambiev, and M. Ohkubo, “Structure preserving signatures and commitments to group elements,” <i>Journal of Cryptology</i>, vol. 29, no. 2. Springer, pp. 363–421, 2016.","ista":"Abe M, Fuchsbauer G, Groth J, Haralambiev K, Ohkubo M. 2016. Structure preserving signatures and commitments to group elements. Journal of Cryptology. 29(2), 363–421.","mla":"Abe, Masayuki, et al. “Structure Preserving Signatures and Commitments to Group Elements.” <i>Journal of Cryptology</i>, vol. 29, no. 2, Springer, 2016, pp. 363–421, doi:<a href=\"https://doi.org/10.1007/s00145-014-9196-7\">10.1007/s00145-014-9196-7</a>.","short":"M. Abe, G. Fuchsbauer, J. Groth, K. Haralambiev, M. Ohkubo, Journal of Cryptology 29 (2016) 363–421.","ama":"Abe M, Fuchsbauer G, Groth J, Haralambiev K, Ohkubo M. Structure preserving signatures and commitments to group elements. <i>Journal of Cryptology</i>. 2016;29(2):363-421. doi:<a href=\"https://doi.org/10.1007/s00145-014-9196-7\">10.1007/s00145-014-9196-7</a>","chicago":"Abe, Masayuki, Georg Fuchsbauer, Jens Groth, Kristiyan Haralambiev, and Miyako Ohkubo. “Structure Preserving Signatures and Commitments to Group Elements.” <i>Journal of Cryptology</i>. Springer, 2016. <a href=\"https://doi.org/10.1007/s00145-014-9196-7\">https://doi.org/10.1007/s00145-014-9196-7</a>.","apa":"Abe, M., Fuchsbauer, G., Groth, J., Haralambiev, K., &#38; Ohkubo, M. (2016). Structure preserving signatures and commitments to group elements. <i>Journal of Cryptology</i>. Springer. <a href=\"https://doi.org/10.1007/s00145-014-9196-7\">https://doi.org/10.1007/s00145-014-9196-7</a>"},"author":[{"last_name":"Abe","first_name":"Masayuki","full_name":"Abe, Masayuki"},{"id":"46B4C3EE-F248-11E8-B48F-1D18A9856A87","last_name":"Fuchsbauer","full_name":"Fuchsbauer, Georg","first_name":"Georg"},{"last_name":"Groth","first_name":"Jens","full_name":"Groth, Jens"},{"last_name":"Haralambiev","first_name":"Kristiyan","full_name":"Haralambiev, Kristiyan"},{"last_name":"Ohkubo","first_name":"Miyako","full_name":"Ohkubo, Miyako"}],"quality_controlled":"1","status":"public","oa_version":"None"},{"project":[{"name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","_id":"25A603A2-B435-11E9-9278-68D0E5697425","grant_number":"281556","call_identifier":"FP7"},{"_id":"25A8E5EA-B435-11E9-9278-68D0E5697425","name":"Cytoskeletal force generation and transduction of leukocytes (FWF)","call_identifier":"FWF","grant_number":"Y 564-B12"}],"acknowledgement":"This work was supported by the Boehringer Ingelheim Fonds, the European Research Council (ERC StG 281556), and a START Award of the Austrian Science Foundation (FWF). We thank Robert Hauschild, Anne Reversat, and Jack Merrin for valuable input and the Imaging Facility of IST Austria for excellent support.","year":"2016","title":"Quantitative analysis of dendritic cell haptotaxis","article_processing_charge":"No","_id":"1597","date_updated":"2021-01-12T06:51:51Z","external_id":{"pmid":["26921962"]},"date_published":"2016-01-01T00:00:00Z","day":"01","status":"public","author":[{"first_name":"Jan","full_name":"Schwarz, Jan","last_name":"Schwarz","id":"346C1EC6-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Michael K","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt"}],"oa_version":"None","volume":570,"date_created":"2018-12-11T11:52:56Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","pmid":1,"doi":"10.1016/bs.mie.2015.11.004","month":"01","intvolume":"       570","ec_funded":1,"acknowledged_ssus":[{"_id":"Bio"}],"page":"567 - 581","type":"journal_article","department":[{"_id":"MiSi"}],"language":[{"iso":"eng"}],"publist_id":"5573","abstract":[{"text":"Chemokines are the main guidance cues directing leukocyte migration. Opposed to early assumptions, chemokines do not necessarily act as soluble cues but are often immobilized within tissues, e.g., dendritic cell migration toward lymphatic vessels is guided by a haptotactic gradient of the chemokine CCL21. Controlled assay systems to quantitatively study haptotaxis in vitro are still missing. In this chapter, we describe an in vitro haptotaxis assay optimized for the unique properties of dendritic cells. The chemokine CCL21 is immobilized in a bioactive state, using laser-assisted protein adsorption by photobleaching. The cells follow this immobilized CCL21 gradient in a haptotaxis chamber, which provides three dimensionally confined migration conditions.","lang":"eng"}],"publication":"Methods in Enzymology","scopus_import":1,"publisher":"Elsevier","citation":{"ama":"Schwarz J, Sixt MK. Quantitative analysis of dendritic cell haptotaxis. <i>Methods in Enzymology</i>. 2016;570:567-581. doi:<a href=\"https://doi.org/10.1016/bs.mie.2015.11.004\">10.1016/bs.mie.2015.11.004</a>","chicago":"Schwarz, Jan, and Michael K Sixt. “Quantitative Analysis of Dendritic Cell Haptotaxis.” <i>Methods in Enzymology</i>. Elsevier, 2016. <a href=\"https://doi.org/10.1016/bs.mie.2015.11.004\">https://doi.org/10.1016/bs.mie.2015.11.004</a>.","apa":"Schwarz, J., &#38; Sixt, M. K. (2016). Quantitative analysis of dendritic cell haptotaxis. <i>Methods in Enzymology</i>. Elsevier. <a href=\"https://doi.org/10.1016/bs.mie.2015.11.004\">https://doi.org/10.1016/bs.mie.2015.11.004</a>","ista":"Schwarz J, Sixt MK. 2016. Quantitative analysis of dendritic cell haptotaxis. Methods in Enzymology. 570, 567–581.","ieee":"J. Schwarz and M. K. Sixt, “Quantitative analysis of dendritic cell haptotaxis,” <i>Methods in Enzymology</i>, vol. 570. Elsevier, pp. 567–581, 2016.","mla":"Schwarz, Jan, and Michael K. Sixt. “Quantitative Analysis of Dendritic Cell Haptotaxis.” <i>Methods in Enzymology</i>, vol. 570, Elsevier, 2016, pp. 567–81, doi:<a href=\"https://doi.org/10.1016/bs.mie.2015.11.004\">10.1016/bs.mie.2015.11.004</a>.","short":"J. Schwarz, M.K. Sixt, Methods in Enzymology 570 (2016) 567–581."},"quality_controlled":"1","publication_status":"published","article_type":"original"},{"abstract":[{"text":"The addition of polysialic acid to N- and/or O-linked glycans, referred to as polysialylation, is a rare posttranslational modification that is mainly known to control the developmental plasticity of the nervous system. Here we show that CCR7, the central chemokine receptor controlling immune cell trafficking to secondary lymphatic organs, carries polysialic acid. This modification is essential for the recognition of the CCR7 ligand CCL21. As a consequence, dendritic cell trafficking is abrogated in polysialyltransferase-deficient mice, manifesting as disturbed lymph node homeostasis and unresponsiveness to inflammatory stimuli. Structure-function analysis of chemokine-receptor interactions reveals that CCL21 adopts an autoinhibited conformation, which is released upon interaction with polysialic acid. Thus, we describe a glycosylation-mediated immune cell trafficking disorder and its mechanistic basis.\r\n","lang":"eng"}],"department":[{"_id":"MiSi"}],"publist_id":"5570","language":[{"iso":"eng"}],"publisher":"American Association for the Advancement of Science","scopus_import":1,"publication":"Science","citation":{"ama":"Kiermaier E, Moussion C, Veldkamp C, et al. Polysialylation controls dendritic cell trafficking by regulating chemokine recognition. <i>Science</i>. 2016;351(6269):186-190. doi:<a href=\"https://doi.org/10.1126/science.aad0512\">10.1126/science.aad0512</a>","chicago":"Kiermaier, Eva, Christine Moussion, Christopher Veldkamp, Rita Gerardy  Schahn, Ingrid de Vries, Larry Williams, Gary Chaffee, et al. “Polysialylation Controls Dendritic Cell Trafficking by Regulating Chemokine Recognition.” <i>Science</i>. American Association for the Advancement of Science, 2016. <a href=\"https://doi.org/10.1126/science.aad0512\">https://doi.org/10.1126/science.aad0512</a>.","apa":"Kiermaier, E., Moussion, C., Veldkamp, C., Gerardy  Schahn, R., de Vries, I., Williams, L., … Sixt, M. K. (2016). Polysialylation controls dendritic cell trafficking by regulating chemokine recognition. <i>Science</i>. American Association for the Advancement of Science. <a href=\"https://doi.org/10.1126/science.aad0512\">https://doi.org/10.1126/science.aad0512</a>","ista":"Kiermaier E, Moussion C, Veldkamp C, Gerardy  Schahn R, de Vries I, Williams L, Chaffee G, Phillips A, Freiberger F, Imre R, Taleski D, Payne R, Braun A, Förster R, Mechtler K, Mühlenhoff M, Volkman B, Sixt MK. 2016. Polysialylation controls dendritic cell trafficking by regulating chemokine recognition. Science. 351(6269), 186–190.","ieee":"E. Kiermaier <i>et al.</i>, “Polysialylation controls dendritic cell trafficking by regulating chemokine recognition,” <i>Science</i>, vol. 351, no. 6269. American Association for the Advancement of Science, pp. 186–190, 2016.","short":"E. Kiermaier, C. Moussion, C. Veldkamp, R. Gerardy  Schahn, I. de Vries, L. Williams, G. Chaffee, A. Phillips, F. Freiberger, R. Imre, D. Taleski, R. Payne, A. Braun, R. Förster, K. Mechtler, M. Mühlenhoff, B. Volkman, M.K. Sixt, Science 351 (2016) 186–190.","mla":"Kiermaier, Eva, et al. “Polysialylation Controls Dendritic Cell Trafficking by Regulating Chemokine Recognition.” <i>Science</i>, vol. 351, no. 6269, American Association for the Advancement of Science, 2016, pp. 186–90, doi:<a href=\"https://doi.org/10.1126/science.aad0512\">10.1126/science.aad0512</a>."},"quality_controlled":"1","article_type":"original","publication_status":"published","intvolume":"       351","month":"01","ec_funded":1,"acknowledged_ssus":[{"_id":"SSU"}],"page":"186 - 190","issue":"6269","main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5583642/","open_access":"1"}],"type":"journal_article","external_id":{"pmid":["26657283"]},"day":"08","date_published":"2016-01-08T00:00:00Z","oa_version":"Submitted Version","author":[{"first_name":"Eva","full_name":"Kiermaier, Eva","orcid":"0000-0001-6165-5738","id":"3EB04B78-F248-11E8-B48F-1D18A9856A87","last_name":"Kiermaier"},{"last_name":"Moussion","id":"3356F664-F248-11E8-B48F-1D18A9856A87","full_name":"Moussion, Christine","first_name":"Christine"},{"first_name":"Christopher","full_name":"Veldkamp, Christopher","last_name":"Veldkamp"},{"last_name":"Gerardy  Schahn","full_name":"Gerardy  Schahn, Rita","first_name":"Rita"},{"first_name":"Ingrid","full_name":"De Vries, Ingrid","last_name":"De Vries","id":"4C7D837E-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Williams, Larry","first_name":"Larry","last_name":"Williams"},{"full_name":"Chaffee, Gary","first_name":"Gary","last_name":"Chaffee"},{"last_name":"Phillips","first_name":"Andrew","full_name":"Phillips, Andrew"},{"last_name":"Freiberger","full_name":"Freiberger, Friedrich","first_name":"Friedrich"},{"last_name":"Imre","first_name":"Richard","full_name":"Imre, Richard"},{"last_name":"Taleski","first_name":"Deni","full_name":"Taleski, Deni"},{"first_name":"Richard","full_name":"Payne, Richard","last_name":"Payne"},{"first_name":"Asolina","full_name":"Braun, Asolina","last_name":"Braun"},{"first_name":"Reinhold","full_name":"Förster, Reinhold","last_name":"Förster"},{"full_name":"Mechtler, Karl","first_name":"Karl","last_name":"Mechtler"},{"last_name":"Mühlenhoff","first_name":"Martina","full_name":"Mühlenhoff, Martina"},{"last_name":"Volkman","full_name":"Volkman, Brian","first_name":"Brian"},{"last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","first_name":"Michael K","full_name":"Sixt, Michael K"}],"status":"public","doi":"10.1126/science.aad0512","pmid":1,"volume":351,"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_created":"2018-12-11T11:52:57Z","project":[{"name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","_id":"25A603A2-B435-11E9-9278-68D0E5697425","grant_number":"281556","call_identifier":"FP7"},{"name":"Stromal Cell-immune Cell Interactions in Health and Disease","_id":"25A76F58-B435-11E9-9278-68D0E5697425","grant_number":"289720","call_identifier":"FP7"},{"_id":"25A8E5EA-B435-11E9-9278-68D0E5697425","name":"Cytoskeletal force generation and transduction of leukocytes (FWF)","call_identifier":"FWF","grant_number":"Y 564-B12"}],"acknowledgement":"We thank S. Schüchner and E. Ogris for kindly providing the antibody to GFP, M. Helmbrecht and A. Huber for providing Nrp2−/− mice, the IST Scientific Support Facilities for excellent services, and J. Renkawitz and K. Vaahtomeri for critically reading the manuscript. ","year":"2016","oa":1,"article_processing_charge":"No","title":"Polysialylation controls dendritic cell trafficking by regulating chemokine recognition","_id":"1599","date_updated":"2021-01-12T06:51:52Z"},{"publication":"Annales Henri Poincare","scopus_import":1,"publisher":"Birkhäuser","language":[{"iso":"eng"}],"publist_id":"5558","department":[{"_id":"LaEr"}],"abstract":[{"lang":"eng","text":"We show that the Anderson model has a transition from localization to delocalization at exactly 2 dimensional growth rate on antitrees with normalized edge weights which are certain discrete graphs. The kinetic part has a one-dimensional structure allowing a description through transfer matrices which involve some Schur complement. For such operators we introduce the notion of having one propagating channel and extend theorems from the theory of one-dimensional Jacobi operators that relate the behavior of transfer matrices with the spectrum. These theorems are then applied to the considered model. In essence, in a certain energy region the kinetic part averages the random potentials along shells and the transfer matrices behave similar as for a one-dimensional operator with random potential of decaying variance. At d dimensional growth for d&gt;2 this effective decay is strong enough to obtain absolutely continuous spectrum, whereas for some uniform d dimensional growth with d&lt;2 one has pure point spectrum in this energy region. At exactly uniform 2 dimensional growth also some singular continuous spectrum appears, at least at small disorder. As a corollary we also obtain a change from singular spectrum (d≤2) to absolutely continuous spectrum (d≥3) for random operators of the type rΔdr+λ on ℤd, where r is an orthogonal radial projection, Δd the discrete adjacency operator (Laplacian) on ℤd and λ a random potential. "}],"publication_status":"published","citation":{"mla":"Sadel, Christian. “Anderson Transition at 2 Dimensional Growth Rate on Antitrees and Spectral Theory for Operators with One Propagating Channel.” <i>Annales Henri Poincare</i>, vol. 17, no. 7, Birkhäuser, 2016, pp. 1631–75, doi:<a href=\"https://doi.org/10.1007/s00023-015-0456-3\">10.1007/s00023-015-0456-3</a>.","short":"C. Sadel, Annales Henri Poincare 17 (2016) 1631–1675.","ieee":"C. Sadel, “Anderson transition at 2 dimensional growth rate on antitrees and spectral theory for operators with one propagating channel,” <i>Annales Henri Poincare</i>, vol. 17, no. 7. Birkhäuser, pp. 1631–1675, 2016.","ista":"Sadel C. 2016. Anderson transition at 2 dimensional growth rate on antitrees and spectral theory for operators with one propagating channel. Annales Henri Poincare. 17(7), 1631–1675.","apa":"Sadel, C. (2016). Anderson transition at 2 dimensional growth rate on antitrees and spectral theory for operators with one propagating channel. <i>Annales Henri Poincare</i>. Birkhäuser. <a href=\"https://doi.org/10.1007/s00023-015-0456-3\">https://doi.org/10.1007/s00023-015-0456-3</a>","chicago":"Sadel, Christian. “Anderson Transition at 2 Dimensional Growth Rate on Antitrees and Spectral Theory for Operators with One Propagating Channel.” <i>Annales Henri Poincare</i>. Birkhäuser, 2016. <a href=\"https://doi.org/10.1007/s00023-015-0456-3\">https://doi.org/10.1007/s00023-015-0456-3</a>.","ama":"Sadel C. Anderson transition at 2 dimensional growth rate on antitrees and spectral theory for operators with one propagating channel. <i>Annales Henri Poincare</i>. 2016;17(7):1631-1675. doi:<a href=\"https://doi.org/10.1007/s00023-015-0456-3\">10.1007/s00023-015-0456-3</a>"},"quality_controlled":"1","issue":"7","ec_funded":1,"page":"1631 - 1675","month":"07","intvolume":"        17","type":"journal_article","main_file_link":[{"open_access":"1","url":"http://arxiv.org/abs/1501.04287"}],"date_published":"2016-07-01T00:00:00Z","day":"01","volume":17,"date_created":"2018-12-11T11:53:00Z","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","doi":"10.1007/s00023-015-0456-3","author":[{"orcid":"0000-0001-8255-3968","full_name":"Sadel, Christian","first_name":"Christian","last_name":"Sadel","id":"4760E9F8-F248-11E8-B48F-1D18A9856A87"}],"status":"public","oa_version":"Preprint","oa":1,"year":"2016","project":[{"call_identifier":"FP7","grant_number":"291734","_id":"25681D80-B435-11E9-9278-68D0E5697425","name":"International IST Postdoc Fellowship Programme"}],"_id":"1608","date_updated":"2021-01-12T06:51:58Z","title":"Anderson transition at 2 dimensional growth rate on antitrees and spectral theory for operators with one propagating channel"},{"abstract":[{"lang":"eng","text":"We prove that whenever A is a 3-conservative relational structure with only binary and unary relations,then the algebra of polymorphisms of A either has no Taylor operation (i.e.,CSP(A)is NP-complete),or it generates an SD(∧) variety (i.e.,CSP(A)has bounded width)."}],"language":[{"iso":"eng"}],"publist_id":"5554","department":[{"_id":"VlKo"}],"day":"01","publisher":"Springer","date_published":"2016-02-01T00:00:00Z","scopus_import":1,"publication":"Algebra Universalis","oa_version":"Preprint","quality_controlled":"1","status":"public","author":[{"first_name":"Alexandr","full_name":"Kazda, Alexandr","last_name":"Kazda","id":"3B32BAA8-F248-11E8-B48F-1D18A9856A87"}],"citation":{"short":"A. Kazda, Algebra Universalis 75 (2016) 75–84.","mla":"Kazda, Alexandr. “CSP for Binary Conservative Relational Structures.” <i>Algebra Universalis</i>, vol. 75, no. 1, Springer, 2016, pp. 75–84, doi:<a href=\"https://doi.org/10.1007/s00012-015-0358-8\">10.1007/s00012-015-0358-8</a>.","ista":"Kazda A. 2016. CSP for binary conservative relational structures. Algebra Universalis. 75(1), 75–84.","ieee":"A. Kazda, “CSP for binary conservative relational structures,” <i>Algebra Universalis</i>, vol. 75, no. 1. Springer, pp. 75–84, 2016.","chicago":"Kazda, Alexandr. “CSP for Binary Conservative Relational Structures.” <i>Algebra Universalis</i>. Springer, 2016. <a href=\"https://doi.org/10.1007/s00012-015-0358-8\">https://doi.org/10.1007/s00012-015-0358-8</a>.","apa":"Kazda, A. (2016). CSP for binary conservative relational structures. <i>Algebra Universalis</i>. Springer. <a href=\"https://doi.org/10.1007/s00012-015-0358-8\">https://doi.org/10.1007/s00012-015-0358-8</a>","ama":"Kazda A. CSP for binary conservative relational structures. <i>Algebra Universalis</i>. 2016;75(1):75-84. doi:<a href=\"https://doi.org/10.1007/s00012-015-0358-8\">10.1007/s00012-015-0358-8</a>"},"doi":"10.1007/s00012-015-0358-8","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","date_created":"2018-12-11T11:53:01Z","publication_status":"published","volume":75,"intvolume":"        75","year":"2016","month":"02","page":"75 - 84","oa":1,"issue":"1","main_file_link":[{"url":"http://arxiv.org/abs/1112.1099","open_access":"1"}],"title":"CSP for binary conservative relational structures","date_updated":"2021-01-12T06:52:00Z","type":"journal_article","_id":"1612"},{"citation":{"ama":"Mungenast A, Siegert S, Tsai L. Modeling Alzheimer’s disease with human induced pluripotent stem (iPS) cells. <i>Molecular and Cellular Neuroscience</i>. 2016;73:13-31. doi:<a href=\"https://doi.org/doi:10.1016/j.mcn.2015.11.010\">doi:10.1016/j.mcn.2015.11.010</a>","apa":"Mungenast, A., Siegert, S., &#38; Tsai, L. (2016). Modeling Alzheimer’s disease with human induced pluripotent stem (iPS) cells. <i>Molecular and Cellular Neuroscience</i>. Academic Press. <a href=\"https://doi.org/doi:10.1016/j.mcn.2015.11.010\">https://doi.org/doi:10.1016/j.mcn.2015.11.010</a>","chicago":"Mungenast, Alison, Sandra Siegert, and Li Tsai. “Modeling Alzheimer’s Disease with Human Induced Pluripotent Stem (IPS) Cells.” <i>Molecular and Cellular Neuroscience</i>. Academic Press, 2016. <a href=\"https://doi.org/doi:10.1016/j.mcn.2015.11.010\">https://doi.org/doi:10.1016/j.mcn.2015.11.010</a>.","ista":"Mungenast A, Siegert S, Tsai L. 2016. Modeling Alzheimer’s disease with human induced pluripotent stem (iPS) cells. Molecular and Cellular Neuroscience. 73, 13–31.","ieee":"A. Mungenast, S. Siegert, and L. Tsai, “Modeling Alzheimer’s disease with human induced pluripotent stem (iPS) cells,” <i>Molecular and Cellular Neuroscience</i>, vol. 73. Academic Press, pp. 13–31, 2016.","short":"A. Mungenast, S. Siegert, L. Tsai, Molecular and Cellular Neuroscience 73 (2016) 13–31.","mla":"Mungenast, Alison, et al. “Modeling Alzheimer’s Disease with Human Induced Pluripotent Stem (IPS) Cells.” <i>Molecular and Cellular Neuroscience</i>, vol. 73, Academic Press, 2016, pp. 13–31, doi:<a href=\"https://doi.org/doi:10.1016/j.mcn.2015.11.010\">doi:10.1016/j.mcn.2015.11.010</a>."},"quality_controlled":"1","publication_status":"published","language":[{"iso":"eng"}],"publist_id":"5553","abstract":[{"text":"In the last decade, induced pluripotent stem (iPS) cells have revolutionized the utility of human in vitro models of neurological disease. The iPS-derived and differentiated cells allow researchers to study the impact of a distinct cell type in health and disease as well as performing therapeutic drug screens on a human genetic background. In particular, clinical trials for Alzheimer's disease (AD) have been often failing. Two of the potential reasons are first, the species gap involved in proceeding from initial discoveries in rodent models to human studies, and second, an unsatisfying patient stratification, meaning subgrouping patients based on the disease severity due to the lack of phenotypic and genetic markers. iPS cells overcome this obstacles and will improve our understanding of disease subtypes in AD. They allow researchers conducting in depth characterization of neural cells from both familial and sporadic AD patients as well as preclinical screens on human cells.\r\n\r\nIn this review, we briefly outline the status quo of iPS cell research in neurological diseases along with the general advantages and pitfalls of these models. We summarize how genome-editing techniques such as CRISPR/Cas will allow researchers to reduce the problem of genomic variability inherent to human studies, followed by recent iPS cell studies relevant to AD. We then focus on current techniques for the differentiation of iPS cells into neural cell types that are relevant to AD research. Finally, we discuss how the generation of three-dimensional cell culture systems will be important for understanding AD phenotypes in a complex cellular milieu, and how both two- and three-dimensional iPS cell models can provide platforms for drug discovery and translational studies into the treatment of AD.","lang":"eng"}],"file_date_updated":"2020-07-14T12:45:07Z","publication":"Molecular and Cellular Neuroscience","file":[{"file_name":"IST-2018-979-v1+1_Mungenast_2015_acceptedManuscript.pdf","date_updated":"2020-07-14T12:45:07Z","date_created":"2018-12-12T10:12:50Z","file_size":632915,"relation":"main_file","file_id":"4970","creator":"system","access_level":"open_access","checksum":"620254114e04d5d6e7f37d15e4b8ace4","content_type":"application/pdf"}],"publisher":"Academic Press","type":"journal_article","ddc":["616"],"month":"06","pubrep_id":"979","intvolume":"        73","page":"13 - 31","extern":"1","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","image":"/images/cc_by_nc_nd.png","short":"CC BY-NC-ND (4.0)","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)"},"author":[{"first_name":"Alison","full_name":"Mungenast, Alison","last_name":"Mungenast"},{"orcid":"0000-0001-8635-0877","first_name":"Sandra","full_name":"Siegert, Sandra","last_name":"Siegert","id":"36ACD32E-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Tsai, Li","first_name":"Li","last_name":"Tsai"}],"status":"public","oa_version":"Submitted Version","volume":73,"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","date_created":"2018-12-11T11:53:02Z","doi":"doi:10.1016/j.mcn.2015.11.010","date_published":"2016-06-01T00:00:00Z","day":"01","title":"Modeling Alzheimer's disease with human induced pluripotent stem (iPS) cells","_id":"1613","date_updated":"2021-01-12T06:52:00Z","has_accepted_license":"1","acknowledgement":"This work was supported by NIH grant R01-AG047661 to LHT. The art in Fig. 1 was created by Julian Wong.","year":"2016","oa":1},{"oa":1,"publication_identifier":{"eissn":["1098-1063"],"issn":["1050-9631"]},"acknowledgement":"The authors thank Jose Guzman for critically reading prior versions of the manuscript. They also thank T. Asenov for\r\nengineering mechanical devices, A. Schlögl for efﬁcient pro-gramming, F. Marr for technical assistance, and E. Kramberger for manuscript editing.","year":"2016","has_accepted_license":"1","date_updated":"2023-10-17T10:02:02Z","_id":"1616","article_processing_charge":"No","title":"Intrinsic membrane properties determine hippocampal differential firing pattern in vivo in anesthetized rats","day":"01","date_published":"2016-05-01T00:00:00Z","doi":"10.1002/hipo.22550","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_created":"2018-12-11T11:53:03Z","volume":26,"oa_version":"Published Version","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","image":"/images/cc_by_nc_nd.png","short":"CC BY-NC-ND (4.0)","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)"},"author":[{"id":"3F3CA136-F248-11E8-B48F-1D18A9856A87","last_name":"Kowalski","full_name":"Kowalski, Janina","first_name":"Janina"},{"id":"3614E438-F248-11E8-B48F-1D18A9856A87","last_name":"Gan","first_name":"Jian","full_name":"Gan, Jian"},{"last_name":"Jonas","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5001-4804","full_name":"Jonas, Peter M","first_name":"Peter M"},{"full_name":"Pernia-Andrade, Alejandro","first_name":"Alejandro","last_name":"Pernia-Andrade","id":"36963E98-F248-11E8-B48F-1D18A9856A87"}],"status":"public","page":"668 - 682","issue":"5","pubrep_id":"469","intvolume":"        26","month":"05","ddc":["570"],"type":"journal_article","publisher":"Wiley","file":[{"date_updated":"2020-07-14T12:45:07Z","file_name":"IST-2016-469-v1+1_Kowalski_et_al-Hippocampus.pdf","file_size":905348,"date_created":"2018-12-12T10:13:47Z","relation":"main_file","file_id":"5033","access_level":"open_access","creator":"system","content_type":"application/pdf","checksum":"284b72b12fbe15474833ed3d4549f86b"}],"publication":"Hippocampus","scopus_import":"1","file_date_updated":"2020-07-14T12:45:07Z","abstract":[{"lang":"eng","text":"The hippocampus plays a key role in learning and memory. Previous studies suggested that the main types of principal neurons, dentate gyrus granule cells (GCs), CA3 pyramidal neurons, and CA1 pyramidal neurons, differ in their activity pattern, with sparse firing in GCs and more frequent firing in CA3 and CA1 pyramidal neurons. It has been assumed but never shown that such different activity may be caused by differential synaptic excitation. To test this hypothesis, we performed high-resolution whole-cell patch-clamp recordings in anesthetized rats in vivo. In contrast to previous in vitro data, both CA3 and CA1 pyramidal neurons fired action potentials spontaneously, with a frequency of ∼3–6 Hz, whereas GCs were silent. Furthermore, both CA3 and CA1 cells primarily fired in bursts. To determine the underlying mechanisms, we quantitatively assessed the frequency of spontaneous excitatory synaptic input, the passive membrane properties, and the active membrane characteristics. Surprisingly, GCs showed comparable synaptic excitation to CA3 and CA1 cells and the highest ratio of excitation versus hyperpolarizing inhibition. Thus, differential synaptic excitation is not responsible for differences in firing. Moreover, the three types of hippocampal neurons markedly differed in their passive properties. While GCs showed the most negative membrane potential, CA3 pyramidal neurons had the highest input resistance and the slowest membrane time constant. The three types of neurons also differed in the active membrane characteristics. GCs showed the highest action potential threshold, but displayed the largest gain of the input-output curves. In conclusion, our results reveal that differential firing of the three main types of hippocampal principal neurons in vivo is not primarily caused by differences in the characteristics of the synaptic input, but by the distinct properties of synaptic integration and input-output transformation."}],"department":[{"_id":"PeJo"}],"publist_id":"5550","language":[{"iso":"eng"}],"publication_status":"published","quality_controlled":"1","citation":{"short":"J. Kowalski, J. Gan, P.M. Jonas, A. Pernia-Andrade, Hippocampus 26 (2016) 668–682.","mla":"Kowalski, Janina, et al. “Intrinsic Membrane Properties Determine Hippocampal Differential Firing Pattern in Vivo in Anesthetized Rats.” <i>Hippocampus</i>, vol. 26, no. 5, Wiley, 2016, pp. 668–82, doi:<a href=\"https://doi.org/10.1002/hipo.22550\">10.1002/hipo.22550</a>.","ieee":"J. Kowalski, J. Gan, P. M. Jonas, and A. Pernia-Andrade, “Intrinsic membrane properties determine hippocampal differential firing pattern in vivo in anesthetized rats,” <i>Hippocampus</i>, vol. 26, no. 5. Wiley, pp. 668–682, 2016.","ista":"Kowalski J, Gan J, Jonas PM, Pernia-Andrade A. 2016. Intrinsic membrane properties determine hippocampal differential firing pattern in vivo in anesthetized rats. Hippocampus. 26(5), 668–682.","chicago":"Kowalski, Janina, Jian Gan, Peter M Jonas, and Alejandro Pernia-Andrade. “Intrinsic Membrane Properties Determine Hippocampal Differential Firing Pattern in Vivo in Anesthetized Rats.” <i>Hippocampus</i>. Wiley, 2016. <a href=\"https://doi.org/10.1002/hipo.22550\">https://doi.org/10.1002/hipo.22550</a>.","apa":"Kowalski, J., Gan, J., Jonas, P. M., &#38; Pernia-Andrade, A. (2016). Intrinsic membrane properties determine hippocampal differential firing pattern in vivo in anesthetized rats. <i>Hippocampus</i>. Wiley. <a href=\"https://doi.org/10.1002/hipo.22550\">https://doi.org/10.1002/hipo.22550</a>","ama":"Kowalski J, Gan J, Jonas PM, Pernia-Andrade A. Intrinsic membrane properties determine hippocampal differential firing pattern in vivo in anesthetized rats. <i>Hippocampus</i>. 2016;26(5):668-682. doi:<a href=\"https://doi.org/10.1002/hipo.22550\">10.1002/hipo.22550</a>"}},{"doi":"10.1016/j.jco.2015.11.003","volume":33,"publication_status":"published","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","date_created":"2018-12-11T11:53:03Z","oa_version":"Submitted Version","citation":{"apa":"Pausinger, F., &#38; Steinerberger, S. (2016). On the discrepancy of jittered sampling. <i>Journal of Complexity</i>. Academic Press. <a href=\"https://doi.org/10.1016/j.jco.2015.11.003\">https://doi.org/10.1016/j.jco.2015.11.003</a>","chicago":"Pausinger, Florian, and Stefan Steinerberger. “On the Discrepancy of Jittered Sampling.” <i>Journal of Complexity</i>. Academic Press, 2016. <a href=\"https://doi.org/10.1016/j.jco.2015.11.003\">https://doi.org/10.1016/j.jco.2015.11.003</a>.","ama":"Pausinger F, Steinerberger S. On the discrepancy of jittered sampling. <i>Journal of Complexity</i>. 2016;33:199-216. doi:<a href=\"https://doi.org/10.1016/j.jco.2015.11.003\">10.1016/j.jco.2015.11.003</a>","mla":"Pausinger, Florian, and Stefan Steinerberger. “On the Discrepancy of Jittered Sampling.” <i>Journal of Complexity</i>, vol. 33, Academic Press, 2016, pp. 199–216, doi:<a href=\"https://doi.org/10.1016/j.jco.2015.11.003\">10.1016/j.jco.2015.11.003</a>.","short":"F. Pausinger, S. Steinerberger, Journal of Complexity 33 (2016) 199–216.","ieee":"F. Pausinger and S. Steinerberger, “On the discrepancy of jittered sampling,” <i>Journal of Complexity</i>, vol. 33. Academic Press, pp. 199–216, 2016.","ista":"Pausinger F, Steinerberger S. 2016. On the discrepancy of jittered sampling. Journal of Complexity. 33, 199–216."},"author":[{"full_name":"Pausinger, Florian","first_name":"Florian","orcid":"0000-0002-8379-3768","id":"2A77D7A2-F248-11E8-B48F-1D18A9856A87","last_name":"Pausinger"},{"last_name":"Steinerberger","full_name":"Steinerberger, Stefan","first_name":"Stefan"}],"status":"public","quality_controlled":"1","publisher":"Academic Press","day":"01","scopus_import":1,"publication":"Journal of Complexity","date_published":"2016-04-01T00:00:00Z","abstract":[{"lang":"eng","text":"We study the discrepancy of jittered sampling sets: such a set P⊂ [0,1]d is generated for fixed m∈ℕ by partitioning [0,1]d into md axis aligned cubes of equal measure and placing a random point inside each of the N=md cubes. We prove that, for N sufficiently large, 1/10 d/N1/2+1/2d ≤EDN∗(P)≤ √d(log N) 1/2/N1/2+1/2d, where the upper bound with an unspecified constant Cd was proven earlier by Beck. Our proof makes crucial use of the sharp Dvoretzky-Kiefer-Wolfowitz inequality and a suitably taylored Bernstein inequality; we have reasons to believe that the upper bound has the sharp scaling in N. Additional heuristics suggest that jittered sampling should be able to improve known bounds on the inverse of the star-discrepancy in the regime N≳dd. We also prove a partition principle showing that every partition of [0,1]d combined with a jittered sampling construction gives rise to a set whose expected squared L2-discrepancy is smaller than that of purely random points."}],"department":[{"_id":"HeEd"}],"language":[{"iso":"eng"}],"publist_id":"5549","_id":"1617","type":"journal_article","date_updated":"2021-01-12T06:52:02Z","main_file_link":[{"open_access":"1","url":"http://arxiv.org/abs/1510.00251"}],"title":"On the discrepancy of jittered sampling","oa":1,"page":"199 - 216","acknowledgement":"We are grateful to the referee whose suggestions greatly improved the quality and clarity of the exposition.","year":"2016","intvolume":"        33","month":"04"},{"month":"02","intvolume":"       342","issue":"1","page":"189 - 216","main_file_link":[{"url":"http://arxiv.org/abs/1410.2352","open_access":"1"}],"type":"journal_article","department":[{"_id":"RoSe"}],"language":[{"iso":"eng"}],"publist_id":"5546","abstract":[{"lang":"eng","text":"We consider the Bardeen–Cooper–Schrieffer free energy functional for particles interacting via a two-body potential on a microscopic scale and in the presence of weak external fields varying on a macroscopic scale. We study the influence of the external fields on the critical temperature. We show that in the limit where the ratio between the microscopic and macroscopic scale tends to zero, the next to leading order of the critical temperature is determined by the lowest eigenvalue of the linearization of the Ginzburg–Landau equation."}],"scopus_import":1,"publication":"Communications in Mathematical Physics","publisher":"Springer","citation":{"apa":"Frank, R., Hainzl, C., Seiringer, R., &#38; Solovej, J. (2016). The external field dependence of the BCS critical temperature. <i>Communications in Mathematical Physics</i>. Springer. <a href=\"https://doi.org/10.1007/s00220-015-2526-2\">https://doi.org/10.1007/s00220-015-2526-2</a>","chicago":"Frank, Rupert, Christian Hainzl, Robert Seiringer, and Jan Solovej. “The External Field Dependence of the BCS Critical Temperature.” <i>Communications in Mathematical Physics</i>. Springer, 2016. <a href=\"https://doi.org/10.1007/s00220-015-2526-2\">https://doi.org/10.1007/s00220-015-2526-2</a>.","ama":"Frank R, Hainzl C, Seiringer R, Solovej J. The external field dependence of the BCS critical temperature. <i>Communications in Mathematical Physics</i>. 2016;342(1):189-216. doi:<a href=\"https://doi.org/10.1007/s00220-015-2526-2\">10.1007/s00220-015-2526-2</a>","mla":"Frank, Rupert, et al. “The External Field Dependence of the BCS Critical Temperature.” <i>Communications in Mathematical Physics</i>, vol. 342, no. 1, Springer, 2016, pp. 189–216, doi:<a href=\"https://doi.org/10.1007/s00220-015-2526-2\">10.1007/s00220-015-2526-2</a>.","short":"R. Frank, C. Hainzl, R. Seiringer, J. Solovej, Communications in Mathematical Physics 342 (2016) 189–216.","ieee":"R. Frank, C. Hainzl, R. Seiringer, and J. Solovej, “The external field dependence of the BCS critical temperature,” <i>Communications in Mathematical Physics</i>, vol. 342, no. 1. Springer, pp. 189–216, 2016.","ista":"Frank R, Hainzl C, Seiringer R, Solovej J. 2016. The external field dependence of the BCS critical temperature. Communications in Mathematical Physics. 342(1), 189–216."},"quality_controlled":"1","publication_status":"published","year":"2016","acknowledgement":"The authors are grateful to I. M. Sigal for useful discussions. Financial support from the US National Science Foundation through Grants PHY-1347399 and DMS-1363432 (R.L.F.), from the Danish council for independent research and from ERC Advanced Grant 321029 (J.P.S.) is acknowledged.","oa":1,"title":"The external field dependence of the BCS critical temperature","_id":"1620","date_updated":"2021-01-12T06:52:03Z","date_published":"2016-02-01T00:00:00Z","day":"01","author":[{"first_name":"Rupert","full_name":"Frank, Rupert","last_name":"Frank"},{"full_name":"Hainzl, Christian","first_name":"Christian","last_name":"Hainzl"},{"id":"4AFD0470-F248-11E8-B48F-1D18A9856A87","last_name":"Seiringer","first_name":"Robert","full_name":"Seiringer, Robert","orcid":"0000-0002-6781-0521"},{"first_name":"Jan","full_name":"Solovej, Jan","last_name":"Solovej"}],"status":"public","oa_version":"Submitted Version","volume":342,"date_created":"2018-12-11T11:53:04Z","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","doi":"10.1007/s00220-015-2526-2"},{"_id":"1622","date_updated":"2021-01-12T06:52:04Z","title":"Fractional Hardy–Lieb–Thirring and related Inequalities for interacting systems","oa":1,"project":[{"name":"International IST Postdoc Fellowship Programme","_id":"25681D80-B435-11E9-9278-68D0E5697425","grant_number":"291734","call_identifier":"FP7"}],"acknowledgement":"We thank Jan  Philip  Solovej, Robert Seiringer and Vladimir Maz’ya for helpful discussions, as well as Rupert Frank\r\nand the anonymous referee for useful comments. Part of this work has been carried out during a visit at the Institut Mittag-Leffler (Stockholm). D.L. acknowledges financial support by the grant KAW 2010.0063 from the Knut and Alice Wallenberg Foundation and the Swedish Research Council grant no. 2013-4734. P.T.N. is supported by the People Programme (Marie Curie Actions) of the European Union’s Seventh Framework Programme (FP7/2007-2013) under REA grant agreement no. 291734. F.P. acknowledges support from the ERC project no. 321029 “The\r\nmathematics of the structure of matter”.","year":"2016","doi":"10.1007/s00205-015-0923-5","volume":219,"date_created":"2018-12-11T11:53:05Z","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","oa_version":"Submitted Version","status":"public","author":[{"last_name":"Lundholm","full_name":"Lundholm, Douglas","first_name":"Douglas"},{"last_name":"Nam","id":"404092F4-F248-11E8-B48F-1D18A9856A87","full_name":"Nam, Phan","first_name":"Phan"},{"full_name":"Portmann, Fabian","first_name":"Fabian","last_name":"Portmann"}],"day":"01","date_published":"2016-03-01T00:00:00Z","type":"journal_article","main_file_link":[{"open_access":"1","url":"http://arxiv.org/abs/1501.04570"}],"ec_funded":1,"page":"1343 - 1382","issue":"3","intvolume":"       219","month":"03","publication_status":"published","citation":{"ama":"Lundholm D, Nam P, Portmann F. Fractional Hardy–Lieb–Thirring and related Inequalities for interacting systems. <i>Archive for Rational Mechanics and Analysis</i>. 2016;219(3):1343-1382. doi:<a href=\"https://doi.org/10.1007/s00205-015-0923-5\">10.1007/s00205-015-0923-5</a>","chicago":"Lundholm, Douglas, Phan Nam, and Fabian Portmann. “Fractional Hardy–Lieb–Thirring and Related Inequalities for Interacting Systems.” <i>Archive for Rational Mechanics and Analysis</i>. Springer, 2016. <a href=\"https://doi.org/10.1007/s00205-015-0923-5\">https://doi.org/10.1007/s00205-015-0923-5</a>.","apa":"Lundholm, D., Nam, P., &#38; Portmann, F. (2016). Fractional Hardy–Lieb–Thirring and related Inequalities for interacting systems. <i>Archive for Rational Mechanics and Analysis</i>. Springer. <a href=\"https://doi.org/10.1007/s00205-015-0923-5\">https://doi.org/10.1007/s00205-015-0923-5</a>","ista":"Lundholm D, Nam P, Portmann F. 2016. Fractional Hardy–Lieb–Thirring and related Inequalities for interacting systems. Archive for Rational Mechanics and Analysis. 219(3), 1343–1382.","ieee":"D. Lundholm, P. Nam, and F. Portmann, “Fractional Hardy–Lieb–Thirring and related Inequalities for interacting systems,” <i>Archive for Rational Mechanics and Analysis</i>, vol. 219, no. 3. Springer, pp. 1343–1382, 2016.","short":"D. Lundholm, P. Nam, F. Portmann, Archive for Rational Mechanics and Analysis 219 (2016) 1343–1382.","mla":"Lundholm, Douglas, et al. “Fractional Hardy–Lieb–Thirring and Related Inequalities for Interacting Systems.” <i>Archive for Rational Mechanics and Analysis</i>, vol. 219, no. 3, Springer, 2016, pp. 1343–82, doi:<a href=\"https://doi.org/10.1007/s00205-015-0923-5\">10.1007/s00205-015-0923-5</a>."},"quality_controlled":"1","publisher":"Springer","scopus_import":1,"publication":"Archive for Rational Mechanics and Analysis","abstract":[{"text":"We prove analogues of the Lieb–Thirring and Hardy–Lieb–Thirring inequalities for many-body quantum systems with fractional kinetic operators and homogeneous interaction potentials, where no anti-symmetry on the wave functions is assumed. These many-body inequalities imply interesting one-body interpolation inequalities, and we show that the corresponding one- and many-body inequalities are actually equivalent in certain cases.","lang":"eng"}],"language":[{"iso":"eng"}],"department":[{"_id":"RoSe"}],"publist_id":"5542"},{"intvolume":"       108","pubrep_id":"465","month":"04","page":"1 - 12","ec_funded":1,"ddc":["576"],"type":"journal_article","abstract":[{"lang":"eng","text":"Ancestral processes are fundamental to modern population genetics and spatial structure has been the subject of intense interest for many years. Despite this interest, almost nothing is known about the distribution of the locations of pedigree or genetic ancestors. Using both spatially continuous and stepping-stone models, we show that the distribution of pedigree ancestors approaches a travelling wave, for which we develop two alternative approximations. The speed and width of the wave are sensitive to the local details of the model. After a short time, genetic ancestors spread far more slowly than pedigree ancestors, ultimately diffusing out with radius ## rather than spreading at constant speed. In contrast to the wave of pedigree ancestors, the spread of genetic ancestry is insensitive to the local details of the models."}],"publist_id":"5524","department":[{"_id":"NiBa"}],"language":[{"iso":"eng"}],"publisher":"Academic Press","file_date_updated":"2020-07-14T12:45:07Z","file":[{"file_id":"4865","creator":"system","access_level":"open_access","content_type":"application/pdf","checksum":"6a65ba187994d4ad86c1c509e0ff482a","file_name":"IST-2016-465-v1+1_1-s2.0-S0040580915001094-main.pdf","date_updated":"2020-07-14T12:45:07Z","file_size":1684043,"date_created":"2018-12-12T10:11:12Z","relation":"main_file"}],"scopus_import":1,"publication":"Theoretical Population Biology","quality_controlled":"1","citation":{"short":"J. Kelleher, A. Etheridge, A. Véber, N.H. Barton, Theoretical Population Biology 108 (2016) 1–12.","mla":"Kelleher, Jerome, et al. “Spread of Pedigree versus Genetic Ancestry in Spatially Distributed Populations.” <i>Theoretical Population Biology</i>, vol. 108, Academic Press, 2016, pp. 1–12, doi:<a href=\"https://doi.org/10.1016/j.tpb.2015.10.008\">10.1016/j.tpb.2015.10.008</a>.","ieee":"J. Kelleher, A. Etheridge, A. Véber, and N. H. Barton, “Spread of pedigree versus genetic ancestry in spatially distributed populations,” <i>Theoretical Population Biology</i>, vol. 108. Academic Press, pp. 1–12, 2016.","ista":"Kelleher J, Etheridge A, Véber A, Barton NH. 2016. Spread of pedigree versus genetic ancestry in spatially distributed populations. Theoretical Population Biology. 108, 1–12.","chicago":"Kelleher, Jerome, Alison Etheridge, Amandine Véber, and Nicholas H Barton. “Spread of Pedigree versus Genetic Ancestry in Spatially Distributed Populations.” <i>Theoretical Population Biology</i>. Academic Press, 2016. <a href=\"https://doi.org/10.1016/j.tpb.2015.10.008\">https://doi.org/10.1016/j.tpb.2015.10.008</a>.","apa":"Kelleher, J., Etheridge, A., Véber, A., &#38; Barton, N. H. (2016). Spread of pedigree versus genetic ancestry in spatially distributed populations. <i>Theoretical Population Biology</i>. Academic Press. <a href=\"https://doi.org/10.1016/j.tpb.2015.10.008\">https://doi.org/10.1016/j.tpb.2015.10.008</a>","ama":"Kelleher J, Etheridge A, Véber A, Barton NH. Spread of pedigree versus genetic ancestry in spatially distributed populations. <i>Theoretical Population Biology</i>. 2016;108:1-12. doi:<a href=\"https://doi.org/10.1016/j.tpb.2015.10.008\">10.1016/j.tpb.2015.10.008</a>"},"publication_status":"published","year":"2016","project":[{"name":"Limits to selection in biology and in evolutionary computation","_id":"25B07788-B435-11E9-9278-68D0E5697425","grant_number":"250152","call_identifier":"FP7"}],"has_accepted_license":"1","oa":1,"title":"Spread of pedigree versus genetic ancestry in spatially distributed populations","date_updated":"2021-01-12T06:52:07Z","_id":"1631","day":"01","date_published":"2016-04-01T00:00:00Z","oa_version":"Published Version","author":[{"last_name":"Kelleher","first_name":"Jerome","full_name":"Kelleher, Jerome"},{"last_name":"Etheridge","first_name":"Alison","full_name":"Etheridge, Alison"},{"last_name":"Véber","full_name":"Véber, Amandine","first_name":"Amandine"},{"id":"4880FE40-F248-11E8-B48F-1D18A9856A87","last_name":"Barton","first_name":"Nicholas H","full_name":"Barton, Nicholas H","orcid":"0000-0002-8548-5240"}],"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"status":"public","doi":"10.1016/j.tpb.2015.10.008","date_created":"2018-12-11T11:53:08Z","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","volume":108},{"title":"A forward genetic screen for new regulators of auxin mediated degradation of auxin transport proteins in Arabidopsis thaliana","date_updated":"2021-01-12T06:52:11Z","_id":"1641","acknowledgement":"European Social Fund (CZ.1.07/2.3.00/20.0043) and the Czech Science Foundation GAČR (GA13-40637S) to JF. ","year":"2016","has_accepted_license":"1","oa":1,"oa_version":"Preprint","status":"public","author":[{"last_name":"Zemová","first_name":"Radka","full_name":"Zemová, Radka"},{"first_name":"Marta","full_name":"Zwiewka, Marta","last_name":"Zwiewka"},{"first_name":"Agnieszka","full_name":"Bielach, Agnieszka","last_name":"Bielach"},{"first_name":"Hélène","full_name":"Robert, Hélène","last_name":"Robert"},{"last_name":"Friml","id":"4159519E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-8302-7596","first_name":"Jirí","full_name":"Friml, Jirí"}],"doi":"10.1007/s00344-015-9553-2","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","date_created":"2018-12-11T11:53:12Z","volume":35,"day":"01","date_published":"2016-06-01T00:00:00Z","ddc":["581"],"type":"journal_article","intvolume":"        35","pubrep_id":"1001","month":"06","page":"465 - 476","issue":"2","quality_controlled":"1","citation":{"apa":"Zemová, R., Zwiewka, M., Bielach, A., Robert, H., &#38; Friml, J. (2016). A forward genetic screen for new regulators of auxin mediated degradation of auxin transport proteins in Arabidopsis thaliana. <i>Journal of Plant Growth Regulation</i>. Springer. <a href=\"https://doi.org/10.1007/s00344-015-9553-2\">https://doi.org/10.1007/s00344-015-9553-2</a>","chicago":"Zemová, Radka, Marta Zwiewka, Agnieszka Bielach, Hélène Robert, and Jiří Friml. “A Forward Genetic Screen for New Regulators of Auxin Mediated Degradation of Auxin Transport Proteins in Arabidopsis Thaliana.” <i>Journal of Plant Growth Regulation</i>. Springer, 2016. <a href=\"https://doi.org/10.1007/s00344-015-9553-2\">https://doi.org/10.1007/s00344-015-9553-2</a>.","ama":"Zemová R, Zwiewka M, Bielach A, Robert H, Friml J. A forward genetic screen for new regulators of auxin mediated degradation of auxin transport proteins in Arabidopsis thaliana. <i>Journal of Plant Growth Regulation</i>. 2016;35(2):465-476. doi:<a href=\"https://doi.org/10.1007/s00344-015-9553-2\">10.1007/s00344-015-9553-2</a>","short":"R. Zemová, M. Zwiewka, A. Bielach, H. Robert, J. Friml, Journal of Plant Growth Regulation 35 (2016) 465–476.","mla":"Zemová, Radka, et al. “A Forward Genetic Screen for New Regulators of Auxin Mediated Degradation of Auxin Transport Proteins in Arabidopsis Thaliana.” <i>Journal of Plant Growth Regulation</i>, vol. 35, no. 2, Springer, 2016, pp. 465–76, doi:<a href=\"https://doi.org/10.1007/s00344-015-9553-2\">10.1007/s00344-015-9553-2</a>.","ista":"Zemová R, Zwiewka M, Bielach A, Robert H, Friml J. 2016. A forward genetic screen for new regulators of auxin mediated degradation of auxin transport proteins in Arabidopsis thaliana. Journal of Plant Growth Regulation. 35(2), 465–476.","ieee":"R. Zemová, M. Zwiewka, A. Bielach, H. Robert, and J. Friml, “A forward genetic screen for new regulators of auxin mediated degradation of auxin transport proteins in Arabidopsis thaliana,” <i>Journal of Plant Growth Regulation</i>, vol. 35, no. 2. Springer, pp. 465–476, 2016."},"publication_status":"published","abstract":[{"text":"The plant hormone auxin (indole-3-acetic acid) is a major regulator of plant growth and development including embryo and root patterning, lateral organ formation and growth responses to environmental stimuli. Auxin is directionally transported from cell to cell by the action of specific auxin influx [AUXIN-RESISTANT1 (AUX1)] and efflux [PIN-FORMED (PIN)] transport regulators, whose polar, subcellular localizations are aligned with the direction of the auxin flow. Auxin itself regulates its own transport by modulation of the expression and subcellular localization of the auxin transporters. Increased auxin levels promote the transcription of PIN2 and AUX1 genes as well as stabilize PIN proteins at the plasma membrane, whereas prolonged auxin exposure increases the turnover of PIN proteins and their degradation in the vacuole. In this study, we applied a forward genetic approach, to identify molecular components playing a role in the auxin-mediated degradation. We generated EMS-mutagenized Arabidopsis PIN2::PIN2:GFP, AUX1::AUX1:YFP eir1aux1 populations and designed a screen for mutants with persistently strong fluorescent signals of the tagged PIN2 and AUX1 after prolonged treatment with the synthetic auxin 2,4-dichlorophenoxyacetic acid (2,4-D). This approach yielded novel auxin degradation mutants defective in trafficking and degradation of PIN2 and AUX1 proteins and established a role for auxin-mediated degradation in plant development.","lang":"eng"}],"language":[{"iso":"eng"}],"publist_id":"5512","department":[{"_id":"JiFr"}],"publisher":"Springer","scopus_import":1,"publication":"Journal of Plant Growth Regulation","file":[{"relation":"main_file","date_updated":"2020-07-14T12:45:08Z","file_name":"IST-2018-1001-v1+1_Zemova_JPlantGrowthRegul_2016_proofs.pdf","file_size":5637591,"date_created":"2018-12-12T10:08:34Z","access_level":"open_access","creator":"system","checksum":"0dc6a300cde6536ceedd2bcdd2060efb","content_type":"application/pdf","file_id":"4695"}],"file_date_updated":"2020-07-14T12:45:08Z"}]
