[{"author":[{"full_name":"Kanbara, Kiyoto","last_name":"Kanbara","first_name":"Kiyoto"},{"full_name":"Okamoto, Keiko","first_name":"Keiko","last_name":"Okamoto"},{"full_name":"Nomura, Sakashi","last_name":"Nomura","first_name":"Sakashi"},{"full_name":"Kaneko, Takeshi","last_name":"Kaneko","first_name":"Takeshi"},{"orcid":"0000-0001-8761-9444","first_name":"Ryuichi","last_name":"Shigemoto","full_name":"Ryuichi Shigemoto","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Azuma, Haruhito","last_name":"Azuma","first_name":"Haruhito"},{"first_name":"Yoji","last_name":"Katsuoka","full_name":"Katsuoka, Yoji"},{"full_name":"Watanabe, Masahiko","last_name":"Watanabe","first_name":"Masahiko"}],"citation":{"short":"K. Kanbara, K. Okamoto, S. Nomura, T. Kaneko, R. Shigemoto, H. Azuma, Y. Katsuoka, M. Watanabe, Journal of Andrology 26 (2005) 485–493.","mla":"Kanbara, Kiyoto, et al. “Cellular Localization of GABA and GABAB Receptor Subunit Proteins during Spermiogenesis in Rat Testis.” <i>Journal of Andrology</i>, vol. 26, no. 4, American Society of Andrology, 2005, pp. 485–93, doi:<a href=\"https://doi.org/10.2164/jandrol.04185\">10.2164/jandrol.04185</a>.","ieee":"K. Kanbara <i>et al.</i>, “Cellular localization of GABA and GABAB receptor subunit proteins during spermiogenesis in rat testis,” <i>Journal of Andrology</i>, vol. 26, no. 4. American Society of Andrology, pp. 485–493, 2005.","apa":"Kanbara, K., Okamoto, K., Nomura, S., Kaneko, T., Shigemoto, R., Azuma, H., … Watanabe, M. (2005). Cellular localization of GABA and GABAB receptor subunit proteins during spermiogenesis in rat testis. <i>Journal of Andrology</i>. American Society of Andrology. <a href=\"https://doi.org/10.2164/jandrol.04185\">https://doi.org/10.2164/jandrol.04185</a>","ista":"Kanbara K, Okamoto K, Nomura S, Kaneko T, Shigemoto R, Azuma H, Katsuoka Y, Watanabe M. 2005. Cellular localization of GABA and GABAB receptor subunit proteins during spermiogenesis in rat testis. Journal of Andrology. 26(4), 485–493.","chicago":"Kanbara, Kiyoto, Keiko Okamoto, Sakashi Nomura, Takeshi Kaneko, Ryuichi Shigemoto, Haruhito Azuma, Yoji Katsuoka, and Masahiko Watanabe. “Cellular Localization of GABA and GABAB Receptor Subunit Proteins during Spermiogenesis in Rat Testis.” <i>Journal of Andrology</i>. American Society of Andrology, 2005. <a href=\"https://doi.org/10.2164/jandrol.04185\">https://doi.org/10.2164/jandrol.04185</a>.","ama":"Kanbara K, Okamoto K, Nomura S, et al. Cellular localization of GABA and GABAB receptor subunit proteins during spermiogenesis in rat testis. <i>Journal of Andrology</i>. 2005;26(4):485-493. doi:<a href=\"https://doi.org/10.2164/jandrol.04185\">10.2164/jandrol.04185</a>"},"quality_controlled":0,"extern":1,"date_updated":"2021-01-12T06:58:50Z","volume":26,"title":"Cellular localization of GABA and GABAB receptor subunit proteins during spermiogenesis in rat testis","publisher":"American Society of Andrology","date_published":"2005-07-01T00:00:00Z","issue":"4","publication_status":"published","month":"07","abstract":[{"lang":"eng","text":"The GABAergic system, a major inhibitory regulator in the central nervous system, may also play important roles in peripheral nonneuronal tissues and cells. Recent studies showed that GABAB receptor is expressed in testis and sperm. To understand the role of the GABAergic system in spermiogenesis, we examined cellular localization of GABA and GABAB receptor subunits in rat spermatids by immunocytochemistry. Immunoreactivity for GABA was detected around acrosomal granules of spermatids during the Golgi and cap phases. GABAB(1) immunoreactivity was observed in the acrosomal vesicle of spermatids in Golgi phase, and during cap phase, this reactivity expanded to the entire region of the acrosome covering the nuclear membrane. The level of reactivity decreased gradually with maturation of spermatids. In contrast, GABAB(2) immunoreactivity was not observed in spermatids during Golgi phase but was detected in the equatorial region during cap phase. Both GABA immunoreactivity and GABAB(2) immunoreactivity were transferred to the residual cytoplasm during the release of spermatozoa. Electron microscopic immunocytochemistry revealed that, during cap phase, GABA and GABAB(1) were distributed within the whole acrosomal vesicle but not in the acrosomal granule. GABAB(2) immunoreactivity was observed in the narrow space between the inner acrosomal and nuclear membrane and was limited to the equatorial region of the spermatid head. These results indicate that the GABAergic system might be involved in regulation of spermiogenesis."}],"day":"01","year":"2005","status":"public","doi":"10.2164/jandrol.04185","page":"485 - 493","type":"journal_article","_id":"2651","date_created":"2018-12-11T11:58:52Z","publication":"Journal of Andrology","publist_id":"4246","intvolume":"        26"},{"date_created":"2018-12-11T11:58:53Z","_id":"2652","type":"journal_article","page":"6775 - 6786","doi":"10.1523/JNEUROSCI.1135-05.2005","status":"public","year":"2005","day":"20","intvolume":"        25","publist_id":"4245","publication":"Journal of Neuroscience","date_updated":"2021-01-12T06:58:50Z","quality_controlled":0,"extern":1,"citation":{"short":"C. Price, B. Cauli, E. Kovács, Á. Kulik, B. Lambolez, R. Shigemoto, M. Capogna, Journal of Neuroscience 25 (2005) 6775–6786.","mla":"Price, Christopher, et al. “Neurogliaform Neurons Form a Novel Inhibitory Network in the Hippocampal CA1 Area.” <i>Journal of Neuroscience</i>, vol. 25, no. 29, Society for Neuroscience, 2005, pp. 6775–86, doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.1135-05.2005\">10.1523/JNEUROSCI.1135-05.2005</a>.","chicago":"Price, Christopher, Bruno Cauli, Endre Kovács, Ákos Kulik, Bertrand Lambolez, Ryuichi Shigemoto, and Marco Capogna. “Neurogliaform Neurons Form a Novel Inhibitory Network in the Hippocampal CA1 Area.” <i>Journal of Neuroscience</i>. Society for Neuroscience, 2005. <a href=\"https://doi.org/10.1523/JNEUROSCI.1135-05.2005\">https://doi.org/10.1523/JNEUROSCI.1135-05.2005</a>.","ama":"Price C, Cauli B, Kovács E, et al. Neurogliaform neurons form a novel inhibitory network in the hippocampal CA1 area. <i>Journal of Neuroscience</i>. 2005;25(29):6775-6786. doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.1135-05.2005\">10.1523/JNEUROSCI.1135-05.2005</a>","ista":"Price C, Cauli B, Kovács E, Kulik Á, Lambolez B, Shigemoto R, Capogna M. 2005. Neurogliaform neurons form a novel inhibitory network in the hippocampal CA1 area. Journal of Neuroscience. 25(29), 6775–6786.","apa":"Price, C., Cauli, B., Kovács, E., Kulik, Á., Lambolez, B., Shigemoto, R., &#38; Capogna, M. (2005). Neurogliaform neurons form a novel inhibitory network in the hippocampal CA1 area. <i>Journal of Neuroscience</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/JNEUROSCI.1135-05.2005\">https://doi.org/10.1523/JNEUROSCI.1135-05.2005</a>","ieee":"C. Price <i>et al.</i>, “Neurogliaform neurons form a novel inhibitory network in the hippocampal CA1 area,” <i>Journal of Neuroscience</i>, vol. 25, no. 29. Society for Neuroscience, pp. 6775–6786, 2005."},"author":[{"last_name":"Price","first_name":"Christopher","full_name":"Price, Christopher J"},{"full_name":"Cauli, Bruno","first_name":"Bruno","last_name":"Cauli"},{"full_name":"Kovács, Endre R","first_name":"Endre","last_name":"Kovács"},{"full_name":"Kulik, Ákos","first_name":"Ákos","last_name":"Kulik"},{"full_name":"Lambolez, Bertrand","last_name":"Lambolez","first_name":"Bertrand"},{"id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","full_name":"Ryuichi Shigemoto","first_name":"Ryuichi","last_name":"Shigemoto","orcid":"0000-0001-8761-9444"},{"first_name":"Marco","last_name":"Capogna","full_name":"Capogna,Marco"}],"abstract":[{"lang":"eng","text":"We studied neurogliaform neurons in the stratum lacunosum moleculare of the CA1 hippocampal area. These interneurons have short stellate dendrites and an extensive axonal arbor mainly located in the stratum lacunosum moleculare. Single-cell reverse transcription-PCR showed that these neurons were GABAergic and that the majority expressed mRNA for neuropeptide Y. Most neurogliaform neurons tested were immunoreactive for α-actinin-2, and many stratum lacunosum moleculare interneurons coexpressed α-actinin-2 and neuropeptide Y. Neurogliaform neurons received monosynaptic, DNQX-sensitive excitatory input from the perforant path, and 40 Hz stimulation of this input evoked EPSCs displaying either depression or initial facilitation, followed by depression. Paired recordings performed between neurogliaform neurons showed that 85% of pairs were electrically connected and 70% were also connected via GABAergic synapses. Injection of sine waveforms into neurons during paired recordings resulted in transmission of the waveforms through the electrical synapse. Unitary IPSCs recorded from neurogliaform pairs readily fatigued, had a slow decay, and had a strong depression of the synaptic response at a 5 Hz stimulation frequency that was antagonized by the GABA B antagonist (2S)-3-[[(1S)-1-(3,4-dichlorophenyl)ethyl]amino-2-hydroxypropyl](phenylmethyl) phosphinic acid (CGP55845). The amplitude of the first IPSC during the 5 Hz stimulation was also increased by CGP55845, suggesting a tonic inhibition of synaptic transmission. A small unitary GABA B-mediated IPSC could also be detected, providing the first evidence for such a component between GABAergic interneurons. Electron microscopic localization of the GABA B1 subunit at neurogliaform synapses revealed the protein in both presynaptic and postsynaptic membranes. Our data disclose a novel interneuronal network well suited for modulating the flow of information between the entorhinal cortex and CA1 hippocampus."}],"publication_status":"published","month":"07","issue":"29","publisher":"Society for Neuroscience","date_published":"2005-07-20T00:00:00Z","title":"Neurogliaform neurons form a novel inhibitory network in the hippocampal CA1 area","volume":25},{"extern":1,"quality_controlled":0,"date_updated":"2021-01-12T06:58:50Z","citation":{"short":"A. Hagiwara, Y. Fukazawa, M. Deguchi Tawarada, T. Ohtsuka, R. Shigemoto, Journal of Comparative Neurology 489 (2005) 195–216.","mla":"Hagiwara, Akari, et al. “Differential Distribution of Release-Related Proteins in the Hippocampal CA3 Area as Revealed by Freeze-Fracture Replica Labeling.” <i>Journal of Comparative Neurology</i>, vol. 489, no. 2, Wiley-Blackwell, 2005, pp. 195–216, doi:<a href=\"https://doi.org/10.1002/cne.20633\">10.1002/cne.20633</a>.","apa":"Hagiwara, A., Fukazawa, Y., Deguchi Tawarada, M., Ohtsuka, T., &#38; Shigemoto, R. (2005). Differential distribution of release-related proteins in the hippocampal CA3 area as revealed by freeze-fracture replica labeling. <i>Journal of Comparative Neurology</i>. Wiley-Blackwell. <a href=\"https://doi.org/10.1002/cne.20633\">https://doi.org/10.1002/cne.20633</a>","chicago":"Hagiwara, Akari, Yugo Fukazawa, Maki Deguchi Tawarada, Toshihisa Ohtsuka, and Ryuichi Shigemoto. “Differential Distribution of Release-Related Proteins in the Hippocampal CA3 Area as Revealed by Freeze-Fracture Replica Labeling.” <i>Journal of Comparative Neurology</i>. Wiley-Blackwell, 2005. <a href=\"https://doi.org/10.1002/cne.20633\">https://doi.org/10.1002/cne.20633</a>.","ista":"Hagiwara A, Fukazawa Y, Deguchi Tawarada M, Ohtsuka T, Shigemoto R. 2005. Differential distribution of release-related proteins in the hippocampal CA3 area as revealed by freeze-fracture replica labeling. Journal of Comparative Neurology. 489(2), 195–216.","ama":"Hagiwara A, Fukazawa Y, Deguchi Tawarada M, Ohtsuka T, Shigemoto R. Differential distribution of release-related proteins in the hippocampal CA3 area as revealed by freeze-fracture replica labeling. <i>Journal of Comparative Neurology</i>. 2005;489(2):195-216. doi:<a href=\"https://doi.org/10.1002/cne.20633\">10.1002/cne.20633</a>","ieee":"A. Hagiwara, Y. Fukazawa, M. Deguchi Tawarada, T. Ohtsuka, and R. Shigemoto, “Differential distribution of release-related proteins in the hippocampal CA3 area as revealed by freeze-fracture replica labeling,” <i>Journal of Comparative Neurology</i>, vol. 489, no. 2. Wiley-Blackwell, pp. 195–216, 2005."},"author":[{"full_name":"Hagiwara, Akari","last_name":"Hagiwara","first_name":"Akari"},{"last_name":"Fukazawa","first_name":"Yugo","full_name":"Fukazawa, Yugo"},{"full_name":"Deguchi-Tawarada, Maki","first_name":"Maki","last_name":"Deguchi Tawarada"},{"full_name":"Ohtsuka, Toshihisa","first_name":"Toshihisa","last_name":"Ohtsuka"},{"first_name":"Ryuichi","last_name":"Shigemoto","orcid":"0000-0001-8761-9444","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","full_name":"Ryuichi Shigemoto"}],"publication_status":"published","month":"08","abstract":[{"text":"Synaptic vesicle release occurs at a specialized membrane domain known as the presynaptic active zone (AZ). Several membrane proteins are involved in the vesicle release processes such as docking, priming, and exocytotic fusion. Cytomatrix at the active zone (CAZ) proteins are structural components of the AZ and are highly concentrated in it. Localization of other release-related proteins including target soluble N-ethylmaleimide-sensitive-factor attachment protein receptor (t-SNARE) proteins, however, has not been well demonstrated in the AZ. Here, we used sodium dodecyl sulfate-digested freeze-fracture replica labeling (SDS-FRL) to analyze quantitatively the distribution of CAZ and t-SNARE proteins in the hippocampal CA3 area. The AZ in replicated membrane was identified by immunolabeling for CAZ proteins (CAZ-associated structural protein [CAST] and Bassoon). Clusters of immunogold particles for these proteins were found on the P-face of presynaptic terminals of the mossy fiber and associational/commissural (AJC) fiber. Co-labeling with CAST revealed distribution of the t-SNARE proteins syntaxin and synaptosomal-associated protein of 25 kDa (SNAP-25) in the AZ as well as in the extrasynaptic membrane surrounding the AZ (SZ). Quantitative analysis demonstrated that the density of immunoparticles for CAST in the AZ was more than 100 times higher than in the SZ, whereas that for syntaxin and SNAP-25 was not significantly different between the AZ and SZ in both the A/C and mossy fiber terminals. These results support the involvement of the t-SNARE proteins in exocytotic fusion in the AZ and the role of CAST in specialization of the membrane domain for the AZ.","lang":"eng"}],"issue":"2","date_published":"2005-08-22T00:00:00Z","publisher":"Wiley-Blackwell","volume":489,"title":"Differential distribution of release-related proteins in the hippocampal CA3 area as revealed by freeze-fracture replica labeling","date_created":"2018-12-11T11:58:53Z","type":"journal_article","_id":"2653","page":"195 - 216","doi":"10.1002/cne.20633","day":"22","year":"2005","status":"public","publist_id":"4244","intvolume":"       489","publication":"Journal of Comparative Neurology"},{"publication":"Journal of Neuroscience","publist_id":"4242","intvolume":"        25","day":"09","page":"10520 - 10536","year":"2005","status":"public","doi":"10.1523/JNEUROSCI.2547-05.2005","_id":"2654","type":"journal_article","date_created":"2018-12-11T11:58:53Z","volume":25,"title":" Metabotropic glutamate receptor 8-expressing nerve terminals target subsets of GABAergic neurons in the hippocampus","date_published":"2005-11-09T00:00:00Z","publisher":"Society for Neuroscience","issue":"45","publication_status":"published","month":"11","abstract":[{"lang":"eng","text":"Presynaptic metabotropic glutamate receptors (mGluRs) show a highly selective expression and subcellular location in nerve terminals modulating neurotransmitter release. We have demonstrated that alternatively spliced variants of mGluR8, mGluR8a and mGluR8b, have an overlapping distribution in the hippocampus, and besides perforant path terminals, they are expressed in the presynaptic active zone of boutons making synapses selectively with several types of GABAergic interneurons, primarily in the stratum oriens. Boutons labeled for mGluR8 formed either type I or type II synapses, and the latter were GABAergic. Some mGluR8-positive boutons also expressed mGluR7 or vasoactive intestinal polypeptide. Interneurons strongly immunopositive for the muscarinic M2 or the mGlu1 receptors were the primary targets of mGluR8-containing terminals in the stratum oriens, but only neurochemically distinct subsets were innervated by mGluR8-enriched terminals. The majority of M2-positive neurons were mGluR8 innervated, but a minority, which expresses somatostatin, was not. Rare neurons coexpressing calretinin and M2 were consistently targeted by mGluR8-positive boutons. In vivo recording and labeling of an mGluR8-decorated and strongly M2-positive interneuron revealed a trilaminar cell with complex spike bursts during theta oscillations and strong discharge during sharp wave/ripple events. The trilaminar cell had a large projection from the CA1 area to the subiculum and a preferential innervation of interneurons in the CA1 area in addition to pyramidal cell somata and dendrites. The postsynaptic interneuron type-specific expression of the high-efficacy presynaptic mGluR8 in both putative glutamatergic and in identified GABAergic terminals predicts a role in adjusting the activity of interneurons depending on the level of network activity."}],"author":[{"full_name":"Ferraguti, Francesco","first_name":"Francesco","last_name":"Ferraguti"},{"last_name":"Klausberger","first_name":"Thomas","full_name":"Klausberger,Thomas"},{"full_name":"Cobden, Philip M","last_name":"Cobden","first_name":"Philip"},{"full_name":"Baude, Agnès","last_name":"Baude","first_name":"Agnès"},{"full_name":"Roberts, John D","first_name":"John","last_name":"Roberts"},{"full_name":"Szűcs, Péter","first_name":"Péter","last_name":"Szűcs"},{"full_name":"Kinoshita, Ayae","last_name":"Kinoshita","first_name":"Ayae"},{"full_name":"Ryuichi Shigemoto","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-8761-9444","last_name":"Shigemoto","first_name":"Ryuichi"},{"full_name":"Somogyi, Péter","first_name":"Péter","last_name":"Somogyi"},{"last_name":"Dalezios","first_name":"Yannis","full_name":"Dalezios, Yannis"}],"citation":{"mla":"Ferraguti, Francesco, et al. “ Metabotropic Glutamate Receptor 8-Expressing Nerve Terminals Target Subsets of GABAergic Neurons in the Hippocampus.” <i>Journal of Neuroscience</i>, vol. 25, no. 45, Society for Neuroscience, 2005, pp. 10520–36, doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.2547-05.2005\">10.1523/JNEUROSCI.2547-05.2005</a>.","short":"F. Ferraguti, T. Klausberger, P. Cobden, A. Baude, J. Roberts, P. Szűcs, A. Kinoshita, R. Shigemoto, P. Somogyi, Y. Dalezios, Journal of Neuroscience 25 (2005) 10520–10536.","ista":"Ferraguti F, Klausberger T, Cobden P, Baude A, Roberts J, Szűcs P, Kinoshita A, Shigemoto R, Somogyi P, Dalezios Y. 2005.  Metabotropic glutamate receptor 8-expressing nerve terminals target subsets of GABAergic neurons in the hippocampus. Journal of Neuroscience. 25(45), 10520–10536.","ama":"Ferraguti F, Klausberger T, Cobden P, et al.  Metabotropic glutamate receptor 8-expressing nerve terminals target subsets of GABAergic neurons in the hippocampus. <i>Journal of Neuroscience</i>. 2005;25(45):10520-10536. doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.2547-05.2005\">10.1523/JNEUROSCI.2547-05.2005</a>","chicago":"Ferraguti, Francesco, Thomas Klausberger, Philip Cobden, Agnès Baude, John Roberts, Péter Szűcs, Ayae Kinoshita, Ryuichi Shigemoto, Péter Somogyi, and Yannis Dalezios. “ Metabotropic Glutamate Receptor 8-Expressing Nerve Terminals Target Subsets of GABAergic Neurons in the Hippocampus.” <i>Journal of Neuroscience</i>. Society for Neuroscience, 2005. <a href=\"https://doi.org/10.1523/JNEUROSCI.2547-05.2005\">https://doi.org/10.1523/JNEUROSCI.2547-05.2005</a>.","apa":"Ferraguti, F., Klausberger, T., Cobden, P., Baude, A., Roberts, J., Szűcs, P., … Dalezios, Y. (2005).  Metabotropic glutamate receptor 8-expressing nerve terminals target subsets of GABAergic neurons in the hippocampus. <i>Journal of Neuroscience</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/JNEUROSCI.2547-05.2005\">https://doi.org/10.1523/JNEUROSCI.2547-05.2005</a>","ieee":"F. Ferraguti <i>et al.</i>, “ Metabotropic glutamate receptor 8-expressing nerve terminals target subsets of GABAergic neurons in the hippocampus,” <i>Journal of Neuroscience</i>, vol. 25, no. 45. Society for Neuroscience, pp. 10520–10536, 2005."},"extern":1,"quality_controlled":0,"date_updated":"2021-01-12T06:58:51Z"},{"volume":25,"title":"Target-cell-specific left-right asymmetry of NMDA receptor content in Schaffer collateral synapses in ε1/NR2A knock-out mice","date_published":"2005-10-05T00:00:00Z","publisher":"Society for Neuroscience","issue":"40","abstract":[{"lang":"eng","text":"Input-dependent left-right asymmetry of NMDA receptor ε2 (NR2B) subunit allocation was discovered in hippocampal Schaffer collateral (Sch) and commissural fiber pyramidal cell synapses (Kawakami et al., 2003). To investigate whether this asymmetrical ε2 allocation is also related to the types of the postsynaptic cells, we compared postembedding immunogold labeling for ε2 in left and right Sch synapses on pyramidal cells and interneurons. To facilitate the detection of ε2 density difference, we used ε1 (NR2A) knock-out (KO) mice, which have a simplified NMDA receptor subunit composition. The labeling density for ε2 but not ζ1 (NR1) and subtype 2/3 glutamate receptor (GluR2/3) in Sch-CA1 pyramidal cell synapses was significantly different between the left and right hippocampus with opposite directions in strata oriens and radiatum; the left to right ratio of ε2 labeling density was 1:1.50 in stratum oriens and 1.44:1 in stratum radiatum. No significant difference, however, was detected in CA1 stratum radiatum between the left and right Sch-GluR4-positive (mostly parvalbumin-positive) and Sch-GluR4-negative interneuron synapses. Consistent with the anatomical asymmetry, the amplitude ratio of NMDA EPSCs to non-NMDA EPSCs in pyramidal cells was approximately two times larger in right than left stratum radiatum and vice versa in stratum oriens of ε1 KO mice. Moreover, the amplitude of long-term potentiation in the Sch-CA1 synapses of left stratum radiatum was significantly larger than that in the right corresponding synapses. These results indicate that the asymmetry of ε2 distribution is target cell specific, resulting in the left-right difference in NMDA receptor content and plasticity in Sch-CA1 pyramidal cell synapses in ε1 KO mice."}],"month":"10","publication_status":"published","author":[{"last_name":"Wu","first_name":"Yue","full_name":"Wu, Yue"},{"full_name":"Kawakami, Ryosuke","last_name":"Kawakami","first_name":"Ryosuke"},{"full_name":"Shinohara, Yoshiaki","first_name":"Yoshiaki","last_name":"Shinohara"},{"full_name":"Fukaya, Masahiro","first_name":"Masahiro","last_name":"Fukaya"},{"last_name":"Sakimura","first_name":"Kenji","full_name":"Sakimura, Kenji"},{"full_name":"Mishina, Masayoshi","first_name":"Masayoshi","last_name":"Mishina"},{"first_name":"Masahiko","last_name":"Watanabe","full_name":"Watanabe, Masahiko"},{"full_name":"Ito, Isao","first_name":"Isao","last_name":"Ito"},{"last_name":"Shigemoto","first_name":"Ryuichi","orcid":"0000-0001-8761-9444","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","full_name":"Ryuichi Shigemoto"}],"citation":{"ieee":"Y. Wu <i>et al.</i>, “Target-cell-specific left-right asymmetry of NMDA receptor content in Schaffer collateral synapses in ε1/NR2A knock-out mice,” <i>Journal of Neuroscience</i>, vol. 25, no. 40. Society for Neuroscience, pp. 9213–9226, 2005.","apa":"Wu, Y., Kawakami, R., Shinohara, Y., Fukaya, M., Sakimura, K., Mishina, M., … Shigemoto, R. (2005). Target-cell-specific left-right asymmetry of NMDA receptor content in Schaffer collateral synapses in ε1/NR2A knock-out mice. <i>Journal of Neuroscience</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/JNEUROSCI.2134-05.2005\">https://doi.org/10.1523/JNEUROSCI.2134-05.2005</a>","ista":"Wu Y, Kawakami R, Shinohara Y, Fukaya M, Sakimura K, Mishina M, Watanabe M, Ito I, Shigemoto R. 2005. Target-cell-specific left-right asymmetry of NMDA receptor content in Schaffer collateral synapses in ε1/NR2A knock-out mice. Journal of Neuroscience. 25(40), 9213–9226.","chicago":"Wu, Yue, Ryosuke Kawakami, Yoshiaki Shinohara, Masahiro Fukaya, Kenji Sakimura, Masayoshi Mishina, Masahiko Watanabe, Isao Ito, and Ryuichi Shigemoto. “Target-Cell-Specific Left-Right Asymmetry of NMDA Receptor Content in Schaffer Collateral Synapses in Ε1/NR2A Knock-out Mice.” <i>Journal of Neuroscience</i>. Society for Neuroscience, 2005. <a href=\"https://doi.org/10.1523/JNEUROSCI.2134-05.2005\">https://doi.org/10.1523/JNEUROSCI.2134-05.2005</a>.","ama":"Wu Y, Kawakami R, Shinohara Y, et al. Target-cell-specific left-right asymmetry of NMDA receptor content in Schaffer collateral synapses in ε1/NR2A knock-out mice. <i>Journal of Neuroscience</i>. 2005;25(40):9213-9226. doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.2134-05.2005\">10.1523/JNEUROSCI.2134-05.2005</a>","short":"Y. Wu, R. Kawakami, Y. Shinohara, M. Fukaya, K. Sakimura, M. Mishina, M. Watanabe, I. Ito, R. Shigemoto, Journal of Neuroscience 25 (2005) 9213–9226.","mla":"Wu, Yue, et al. “Target-Cell-Specific Left-Right Asymmetry of NMDA Receptor Content in Schaffer Collateral Synapses in Ε1/NR2A Knock-out Mice.” <i>Journal of Neuroscience</i>, vol. 25, no. 40, Society for Neuroscience, 2005, pp. 9213–26, doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.2134-05.2005\">10.1523/JNEUROSCI.2134-05.2005</a>."},"date_updated":"2021-01-12T06:58:51Z","extern":1,"quality_controlled":0,"publication":"Journal of Neuroscience","intvolume":"        25","publist_id":"4243","status":"public","day":"05","doi":"10.1523/JNEUROSCI.2134-05.2005","year":"2005","page":"9213 - 9226","_id":"2655","type":"journal_article","date_created":"2018-12-11T11:58:54Z"},{"quality_controlled":0,"extern":1,"date_updated":"2021-01-12T06:58:51Z","citation":{"ieee":"Y. Feng <i>et al.</i>, “Morphological evidence for GABA/glycine-cocontaining terminals in synaptic contact with neurokinin-1 receptor-expressing neurons in the sacral dorsal commissural nucleus of the rat,” <i>Neuroscience Letters</i>, vol. 388, no. 3. Elsevier, pp. 144–148, 2005.","ama":"Feng Y, Li Y, Wang W, et al. Morphological evidence for GABA/glycine-cocontaining terminals in synaptic contact with neurokinin-1 receptor-expressing neurons in the sacral dorsal commissural nucleus of the rat. <i>Neuroscience Letters</i>. 2005;388(3):144-148. doi:<a href=\"https://doi.org/10.1016/j.neulet.2005.06.068\">10.1016/j.neulet.2005.06.068</a>","ista":"Feng Y, Li Y, Wang W, Wu S, Chen T, Shigemoto R, Mizuno N. 2005. Morphological evidence for GABA/glycine-cocontaining terminals in synaptic contact with neurokinin-1 receptor-expressing neurons in the sacral dorsal commissural nucleus of the rat. Neuroscience Letters. 388(3), 144–148.","chicago":"Feng, Yu, Yun Li, Wen Wang, Sheng Wu, Tao Chen, Ryuichi Shigemoto, and Noboru Mizuno. “Morphological Evidence for GABA/Glycine-Cocontaining Terminals in Synaptic Contact with Neurokinin-1 Receptor-Expressing Neurons in the Sacral Dorsal Commissural Nucleus of the Rat.” <i>Neuroscience Letters</i>. Elsevier, 2005. <a href=\"https://doi.org/10.1016/j.neulet.2005.06.068\">https://doi.org/10.1016/j.neulet.2005.06.068</a>.","apa":"Feng, Y., Li, Y., Wang, W., Wu, S., Chen, T., Shigemoto, R., &#38; Mizuno, N. (2005). Morphological evidence for GABA/glycine-cocontaining terminals in synaptic contact with neurokinin-1 receptor-expressing neurons in the sacral dorsal commissural nucleus of the rat. <i>Neuroscience Letters</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.neulet.2005.06.068\">https://doi.org/10.1016/j.neulet.2005.06.068</a>","mla":"Feng, Yu, et al. “Morphological Evidence for GABA/Glycine-Cocontaining Terminals in Synaptic Contact with Neurokinin-1 Receptor-Expressing Neurons in the Sacral Dorsal Commissural Nucleus of the Rat.” <i>Neuroscience Letters</i>, vol. 388, no. 3, Elsevier, 2005, pp. 144–48, doi:<a href=\"https://doi.org/10.1016/j.neulet.2005.06.068\">10.1016/j.neulet.2005.06.068</a>.","short":"Y. Feng, Y. Li, W. Wang, S. Wu, T. Chen, R. Shigemoto, N. Mizuno, Neuroscience Letters 388 (2005) 144–148."},"author":[{"last_name":"Feng","first_name":"Yu","full_name":"Feng, Yu-Peng"},{"first_name":"Yun","last_name":"Li","full_name":"Li, Yun-Qing"},{"full_name":"Wang, Wen","first_name":"Wen","last_name":"Wang"},{"first_name":"Sheng","last_name":"Wu","full_name":"Wu, Sheng-Xi"},{"full_name":"Chen, Tao","first_name":"Tao","last_name":"Chen"},{"orcid":"0000-0001-8761-9444","last_name":"Shigemoto","first_name":"Ryuichi","full_name":"Ryuichi Shigemoto","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Noboru","last_name":"Mizuno","full_name":"Mizuno, Noboru"}],"publication_status":"published","month":"11","abstract":[{"lang":"eng","text":"Previous studies have shown that neurons in the sacral dorsal commissural nucleus (SDCN) express neurokinin-1 receptor (NK1R) and can be modulated by the co-release of GABA and glycine (Gly) from single presynaptic terminal. These results raise the possibility that GABA/Gly-cocontaining terminals might make synaptic contacts with NK1R-expressing neurons in the SDCN. In order to provide morphological evidence for this hypothesis, the triple-immunohistochemical studies were performed in the SDCN. Triple-immunofluorescence histochemical study showed that some axon terminals in close association with NK1R-immunopositive (NK1R-ip) neurons in the SDCN were immunopositive for both glutamic acid decarboxylase (GAD) and glycine transporter 2 (GlyT2). In electron microscopic dual- and triple-immunohistochemistry for GAD/GlyT2, GAD/NK1R, GlyT2/NK1R, or GAD/GlyT2/NK1R also revealed dually labeled (GAD/GlyT2-ip) synaptic terminals upon SDCN neurons, as well as GAD- and/or GlyT2-ip axon terminals in synaptic contact with NK1R-ip SDCN neurons. These results suggested that some synaptic terminals upon NK1R-expressing SDCN neurons co-released both GABA and Gly."}],"issue":"3","date_published":"2005-11-18T00:00:00Z","publisher":"Elsevier","volume":388,"title":"Morphological evidence for GABA/glycine-cocontaining terminals in synaptic contact with neurokinin-1 receptor-expressing neurons in the sacral dorsal commissural nucleus of the rat","date_created":"2018-12-11T11:58:54Z","type":"journal_article","_id":"2656","page":"144 - 148","doi":"10.1016/j.neulet.2005.06.068","day":"18","year":"2005","status":"public","publist_id":"4241","intvolume":"       388","publication":"Neuroscience Letters"},{"page":"3241 - 3254","doi":"10.1111/j.1460-9568.2005.04488.x","status":"public","day":"01","year":"2005","_id":"2658","type":"journal_article","date_created":"2018-12-11T11:58:55Z","publication":"European Journal of Neuroscience","intvolume":"        22","publist_id":"4240","author":[{"full_name":"Kaneda, Katsuyuki","first_name":"Katsuyuki","last_name":"Kaneda"},{"last_name":"Tachibana","first_name":"Yoshihisa","full_name":"Tachibana, Yoshihisa"},{"first_name":"Michiko","last_name":"Imanishi","full_name":"Imanishi, Michiko"},{"first_name":"Hitoshi","last_name":"Kita","full_name":"Kita, Hitoshi"},{"orcid":"0000-0001-8761-9444","last_name":"Shigemoto","first_name":"Ryuichi","full_name":"Ryuichi Shigemoto","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Atsushi","last_name":"Nambu","full_name":"Nambu, Atsushi"},{"last_name":"Takada","first_name":"Masahiko","full_name":"Takada, Masahiko"}],"citation":{"mla":"Kaneda, Katsuyuki, et al. “Down-Regulation of Metabotropic Glutamate Receptor 1α in Globus Pallidus and Substantia Nigra of Parkinsonian Monkeys.” <i>European Journal of Neuroscience</i>, vol. 22, no. 12, Wiley-Blackwell, 2005, pp. 3241–54, doi:<a href=\"https://doi.org/10.1111/j.1460-9568.2005.04488.x\">10.1111/j.1460-9568.2005.04488.x</a>.","short":"K. Kaneda, Y. Tachibana, M. Imanishi, H. Kita, R. Shigemoto, A. Nambu, M. Takada, European Journal of Neuroscience 22 (2005) 3241–3254.","ista":"Kaneda K, Tachibana Y, Imanishi M, Kita H, Shigemoto R, Nambu A, Takada M. 2005. Down-regulation of metabotropic glutamate receptor 1α in globus pallidus and substantia nigra of parkinsonian monkeys. European Journal of Neuroscience. 22(12), 3241–3254.","ama":"Kaneda K, Tachibana Y, Imanishi M, et al. Down-regulation of metabotropic glutamate receptor 1α in globus pallidus and substantia nigra of parkinsonian monkeys. <i>European Journal of Neuroscience</i>. 2005;22(12):3241-3254. doi:<a href=\"https://doi.org/10.1111/j.1460-9568.2005.04488.x\">10.1111/j.1460-9568.2005.04488.x</a>","chicago":"Kaneda, Katsuyuki, Yoshihisa Tachibana, Michiko Imanishi, Hitoshi Kita, Ryuichi Shigemoto, Atsushi Nambu, and Masahiko Takada. “Down-Regulation of Metabotropic Glutamate Receptor 1α in Globus Pallidus and Substantia Nigra of Parkinsonian Monkeys.” <i>European Journal of Neuroscience</i>. Wiley-Blackwell, 2005. <a href=\"https://doi.org/10.1111/j.1460-9568.2005.04488.x\">https://doi.org/10.1111/j.1460-9568.2005.04488.x</a>.","apa":"Kaneda, K., Tachibana, Y., Imanishi, M., Kita, H., Shigemoto, R., Nambu, A., &#38; Takada, M. (2005). Down-regulation of metabotropic glutamate receptor 1α in globus pallidus and substantia nigra of parkinsonian monkeys. <i>European Journal of Neuroscience</i>. Wiley-Blackwell. <a href=\"https://doi.org/10.1111/j.1460-9568.2005.04488.x\">https://doi.org/10.1111/j.1460-9568.2005.04488.x</a>","ieee":"K. Kaneda <i>et al.</i>, “Down-regulation of metabotropic glutamate receptor 1α in globus pallidus and substantia nigra of parkinsonian monkeys,” <i>European Journal of Neuroscience</i>, vol. 22, no. 12. Wiley-Blackwell, pp. 3241–3254, 2005."},"date_updated":"2021-01-12T06:58:52Z","extern":1,"quality_controlled":0,"title":"Down-regulation of metabotropic glutamate receptor 1α in globus pallidus and substantia nigra of parkinsonian monkeys","volume":22,"publisher":"Wiley-Blackwell","date_published":"2005-12-01T00:00:00Z","issue":"12","abstract":[{"lang":"eng","text":"Enhanced glutamatergic neurotransmission via the subthalamopallidal or subthalamonigral projection seems crucial for developing parkinsonian motor signs. In the present study, the possible changes in the expression of metabotropic glutamate receptors (mGluRs) were examined in the basal ganglia of a primate model for Parkinson's disease. When the patterns of immunohistochemical localization of mGluRs in monkeys administered systemically with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) were analysed in comparison with normal controls, we found that expression of mGluR1α, but not of other subtypes, was significantly reduced in the internal and external segments of the globus pallidus and the substantia nigra pars reticulata. To elucidate the functional role of mGluR1 in the control of pallidal neuron activity, extracellular unit recordings combined with intrapallidal microinjections of mGluR1-related agents were then performed in normal and parkinsonian monkeys. In normal awake conditions, the spontaneous firing rates of neurons in the pallidal complex were increased by DHPG, a selective agonist of group I mGluRs, whereas they were decreased by AIDA, a selective antagonist of group I mGluRs, or LY367385, a selective antagonist of mGluR1. These electrophysiological data strongly indicate that the excitatory mechanism of pallidal neurons by glutamate is mediated at least partly through mGluR1. The effects of the mGluR1-related agents on neuronal firing in the internal pallidal segment became rather obscure after MPTP treatment. Our results suggest that the specific down-regulation of pallidal and nigral mGluR1 ot in the parkinsonian state may exert a compensatory action to reverse the overactivity of the subthalamic nucleus-derived glutamatergic input that is generated in the disease."}],"month":"12","publication_status":"published"},{"date_created":"2018-12-11T11:59:22Z","type":"journal_article","_id":"2743","year":"2005","page":"247 - 267","doi":"10.1007/s00023-005-0205-0","status":"public","day":"01","publist_id":"4149","intvolume":"         6","publication":"Annales Henri Poincare","quality_controlled":0,"extern":1,"date_updated":"2021-01-12T06:59:24Z","citation":{"ieee":"L. Erdös, D. Hasler, and J. Solovej, “Existence of the D0-D4 bound state: A detailed proof,” <i>Annales Henri Poincare</i>, vol. 6, no. 2. Birkhäuser, pp. 247–267, 2005.","apa":"Erdös, L., Hasler, D., &#38; Solovej, J. (2005). Existence of the D0-D4 bound state: A detailed proof. <i>Annales Henri Poincare</i>. Birkhäuser. <a href=\"https://doi.org/10.1007/s00023-005-0205-0\">https://doi.org/10.1007/s00023-005-0205-0</a>","chicago":"Erdös, László, David Hasler, and Jan Solovej. “Existence of the D0-D4 Bound State: A Detailed Proof.” <i>Annales Henri Poincare</i>. Birkhäuser, 2005. <a href=\"https://doi.org/10.1007/s00023-005-0205-0\">https://doi.org/10.1007/s00023-005-0205-0</a>.","ista":"Erdös L, Hasler D, Solovej J. 2005. Existence of the D0-D4 bound state: A detailed proof. Annales Henri Poincare. 6(2), 247–267.","ama":"Erdös L, Hasler D, Solovej J. Existence of the D0-D4 bound state: A detailed proof. <i>Annales Henri Poincare</i>. 2005;6(2):247-267. doi:<a href=\"https://doi.org/10.1007/s00023-005-0205-0\">10.1007/s00023-005-0205-0</a>","short":"L. Erdös, D. Hasler, J. Solovej, Annales Henri Poincare 6 (2005) 247–267.","mla":"Erdös, László, et al. “Existence of the D0-D4 Bound State: A Detailed Proof.” <i>Annales Henri Poincare</i>, vol. 6, no. 2, Birkhäuser, 2005, pp. 247–67, doi:<a href=\"https://doi.org/10.1007/s00023-005-0205-0\">10.1007/s00023-005-0205-0</a>."},"author":[{"last_name":"Erdös","first_name":"László","orcid":"0000-0001-5366-9603","id":"4DBD5372-F248-11E8-B48F-1D18A9856A87","full_name":"László Erdös"},{"full_name":"Hasler, David G","first_name":"David","last_name":"Hasler"},{"full_name":"Solovej, Jan P","first_name":"Jan","last_name":"Solovej"}],"month":"04","publication_status":"published","abstract":[{"lang":"eng","text":"We consider the supersymmetric quantum mechanical system which is obtained by dimensionally reducing d = 6, N = 1 supersymmetric gauge theory with gauge group U(1) and a single charged hypermultiplet. Using the deformation method and ideas introduced by Porrati and Rozenberg [1], we present a detailed proof of the existence of a normalizable ground state for this system."}],"issue":"2","date_published":"2005-04-01T00:00:00Z","publisher":"Birkhäuser","title":"Existence of the D0-D4 bound state: A detailed proof","volume":6},{"author":[{"full_name":"Eng, David","last_name":"Eng","first_name":"David"},{"full_name":"László Erdös","id":"4DBD5372-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5366-9603","last_name":"Erdös","first_name":"László"}],"citation":{"mla":"Eng, David, and László Erdös. “The Linear Boltzmann Equation as the Low Density Limit of a Random Schrödinger Equation.” <i>Reviews in Mathematical Physics</i>, vol. 17, no. 6, World Scientific Publishing, 2005, pp. 669–743, doi:<a href=\"https://doi.org/10.1142/S0129055X0500242X\">10.1142/S0129055X0500242X</a>.","short":"D. Eng, L. Erdös, Reviews in Mathematical Physics 17 (2005) 669–743.","ieee":"D. Eng and L. Erdös, “The linear Boltzmann equation as the low density limit of a random Schrödinger equation,” <i>Reviews in Mathematical Physics</i>, vol. 17, no. 6. World Scientific Publishing, pp. 669–743, 2005.","ama":"Eng D, Erdös L. The linear Boltzmann equation as the low density limit of a random Schrödinger equation. <i>Reviews in Mathematical Physics</i>. 2005;17(6):669-743. doi:<a href=\"https://doi.org/10.1142/S0129055X0500242X\">10.1142/S0129055X0500242X</a>","ista":"Eng D, Erdös L. 2005. The linear Boltzmann equation as the low density limit of a random Schrödinger equation. Reviews in Mathematical Physics. 17(6), 669–743.","chicago":"Eng, David, and László Erdös. “The Linear Boltzmann Equation as the Low Density Limit of a Random Schrödinger Equation.” <i>Reviews in Mathematical Physics</i>. World Scientific Publishing, 2005. <a href=\"https://doi.org/10.1142/S0129055X0500242X\">https://doi.org/10.1142/S0129055X0500242X</a>.","apa":"Eng, D., &#38; Erdös, L. (2005). The linear Boltzmann equation as the low density limit of a random Schrödinger equation. <i>Reviews in Mathematical Physics</i>. World Scientific Publishing. <a href=\"https://doi.org/10.1142/S0129055X0500242X\">https://doi.org/10.1142/S0129055X0500242X</a>"},"quality_controlled":0,"extern":1,"date_updated":"2021-01-12T06:59:25Z","title":"The linear Boltzmann equation as the low density limit of a random Schrödinger equation","volume":17,"publisher":"World Scientific Publishing","date_published":"2005-07-01T00:00:00Z","issue":"6","month":"07","publication_status":"published","abstract":[{"text":"We study the long time evolution of a quantum particle interacting with a random potential in the Boltzmann-Grad low density limit. We prove that the phase space density of the quantum evolution defined through the Husimi function converges weakly to a linear Boltzmann equation. The Boltzmann collision kernel is given by the full quantum scattering cross-section of the obstacle potential.","lang":"eng"}],"status":"public","doi":"10.1142/S0129055X0500242X","day":"01","year":"2005","page":"669 - 743","type":"journal_article","_id":"2744","date_created":"2018-12-11T11:59:22Z","publication":"Reviews in Mathematical Physics","publist_id":"4148","intvolume":"        17"},{"title":"Turbulence regeneration in pipe flow at moderate reynolds numbers","volume":95,"publisher":"American Physical Society","date_published":"2005-11-17T00:00:00Z","issue":"21","publication_status":"published","month":"11","abstract":[{"lang":"eng","text":"We present the results of an experimental investigation into the nature and structure of turbulent pipe flow at moderate Reynolds numbers. A turbulence regeneration mechanism is identified which sustains a symmetric traveling wave within the flow. The periodicity of the mechanism allows comparison to the wavelength of numerically observed exact traveling wave solutions and close agreement is found. The advection speed of the upstream turbulence laminar interface in the experimental flow is observed to form a lower bound on the phase velocities of the exact traveling wave solutions. Overall our observations suggest that the dynamics of the turbulent flow at moderate Reynolds numbers are governed by unstable nonlinear traveling waves."}],"author":[{"first_name":"Björn","last_name":"Hof","orcid":"0000-0003-2057-2754","id":"3A374330-F248-11E8-B48F-1D18A9856A87","full_name":"Björn Hof"},{"first_name":"Casimir","last_name":"Van Doorne","full_name":"van Doorne, Casimir W"},{"first_name":"Jerry","last_name":"Westerweel","full_name":"Westerweel, Jerry"},{"last_name":"Nieuwstadt","first_name":"Frans","full_name":"Nieuwstadt, Frans T"}],"citation":{"ista":"Hof B, Van Doorne C, Westerweel J, Nieuwstadt F. 2005. Turbulence regeneration in pipe flow at moderate reynolds numbers. Physical Review Letters. 95(21).","ama":"Hof B, Van Doorne C, Westerweel J, Nieuwstadt F. Turbulence regeneration in pipe flow at moderate reynolds numbers. <i>Physical Review Letters</i>. 2005;95(21). doi:<a href=\"https://doi.org/10.1103/PhysRevLett.95.214502\">10.1103/PhysRevLett.95.214502</a>","chicago":"Hof, Björn, Casimir Van Doorne, Jerry Westerweel, and Frans Nieuwstadt. “Turbulence Regeneration in Pipe Flow at Moderate Reynolds Numbers.” <i>Physical Review Letters</i>. American Physical Society, 2005. <a href=\"https://doi.org/10.1103/PhysRevLett.95.214502\">https://doi.org/10.1103/PhysRevLett.95.214502</a>.","apa":"Hof, B., Van Doorne, C., Westerweel, J., &#38; Nieuwstadt, F. (2005). Turbulence regeneration in pipe flow at moderate reynolds numbers. <i>Physical Review Letters</i>. American Physical Society. <a href=\"https://doi.org/10.1103/PhysRevLett.95.214502\">https://doi.org/10.1103/PhysRevLett.95.214502</a>","ieee":"B. Hof, C. Van Doorne, J. Westerweel, and F. Nieuwstadt, “Turbulence regeneration in pipe flow at moderate reynolds numbers,” <i>Physical Review Letters</i>, vol. 95, no. 21. American Physical Society, 2005.","mla":"Hof, Björn, et al. “Turbulence Regeneration in Pipe Flow at Moderate Reynolds Numbers.” <i>Physical Review Letters</i>, vol. 95, no. 21, American Physical Society, 2005, doi:<a href=\"https://doi.org/10.1103/PhysRevLett.95.214502\">10.1103/PhysRevLett.95.214502</a>.","short":"B. Hof, C. Van Doorne, J. Westerweel, F. Nieuwstadt, Physical Review Letters 95 (2005)."},"extern":1,"quality_controlled":0,"date_updated":"2021-01-12T06:59:43Z","publication":"Physical Review Letters","publist_id":"4101","intvolume":"        95","doi":"10.1103/PhysRevLett.95.214502","day":"17","year":"2005","status":"public","type":"journal_article","_id":"2788","date_created":"2018-12-11T11:59:36Z"},{"abstract":[{"lang":"eng","text":"Transitional pipe flow is investigated in two different experimental set-ups. In the first the stability threshold and the initial growth of localized perturbations are studied. Good agreement is found with an earlier investigation of the transition threshold. The measurement technique applied in the last part of this study allows the reconstruction of the streamwise vorticity in a turbulent puff."}],"publication_status":"published","month":"09","date_published":"2005-09-19T00:00:00Z","publisher":"Springer","title":"Transition to turbulence in pipe flow","volume":77,"date_updated":"2021-01-12T06:59:43Z","quality_controlled":0,"extern":1,"citation":{"mla":"Hof, Björn. “Transition to Turbulence in Pipe Flow.” <i>Fluid Mechanics and Its Applications</i>, vol. 77, Springer, 2005, pp. 221–31, doi:<a href=\"https://doi.org/10.1007/1-4020-4049-0_12\">10.1007/1-4020-4049-0_12</a>.","short":"B. Hof, Fluid Mechanics and Its Applications 77 (2005) 221–231.","chicago":"Hof, Björn. “Transition to Turbulence in Pipe Flow.” <i>Fluid Mechanics and Its Applications</i>. Springer, 2005. <a href=\"https://doi.org/10.1007/1-4020-4049-0_12\">https://doi.org/10.1007/1-4020-4049-0_12</a>.","ista":"Hof B. 2005. Transition to turbulence in pipe flow. Fluid Mechanics and its Applications. 77, 221–231.","ama":"Hof B. Transition to turbulence in pipe flow. <i>Fluid Mechanics and its Applications</i>. 2005;77:221-231. doi:<a href=\"https://doi.org/10.1007/1-4020-4049-0_12\">10.1007/1-4020-4049-0_12</a>","apa":"Hof, B. (2005). Transition to turbulence in pipe flow. <i>Fluid Mechanics and Its Applications</i>. Springer. <a href=\"https://doi.org/10.1007/1-4020-4049-0_12\">https://doi.org/10.1007/1-4020-4049-0_12</a>","ieee":"B. Hof, “Transition to turbulence in pipe flow,” <i>Fluid Mechanics and its Applications</i>, vol. 77. Springer, pp. 221–231, 2005."},"author":[{"orcid":"0000-0003-2057-2754","last_name":"Hof","first_name":"Björn","full_name":"Björn Hof","id":"3A374330-F248-11E8-B48F-1D18A9856A87"}],"intvolume":"        77","publist_id":"4100","publication":"Fluid Mechanics and its Applications","date_created":"2018-12-11T11:59:36Z","_id":"2789","type":"journal_article","doi":"10.1007/1-4020-4049-0_12","page":"221 - 231","day":"19","year":"2005","status":"public"},{"day":"25","status":"public","page":"193 - 201","year":"2005","doi":"10.1017/S0022112005006762","date_created":"2018-12-11T11:59:37Z","_id":"2790","type":"journal_article","intvolume":"       545","publist_id":"4099","publication":"Journal of Fluid Mechanics","author":[{"full_name":"Björn Hof","id":"3A374330-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2057-2754","first_name":"Björn","last_name":"Hof"},{"first_name":"Anne","last_name":"Juel","full_name":"Juel, Anne"},{"last_name":"Mullin","first_name":"Tom","full_name":"Mullin, Tom P"}],"date_updated":"2021-01-12T06:59:44Z","extern":1,"quality_controlled":0,"citation":{"ieee":"B. Hof, A. Juel, and T. Mullin, “Magnetohydrodynamic damping of oscillations in low-Prandtl-number convection,” <i>Journal of Fluid Mechanics</i>, vol. 545. Cambridge University Press, pp. 193–201, 2005.","apa":"Hof, B., Juel, A., &#38; Mullin, T. (2005). Magnetohydrodynamic damping of oscillations in low-Prandtl-number convection. <i>Journal of Fluid Mechanics</i>. Cambridge University Press. <a href=\"https://doi.org/10.1017/S0022112005006762\">https://doi.org/10.1017/S0022112005006762</a>","chicago":"Hof, Björn, Anne Juel, and Tom Mullin. “Magnetohydrodynamic Damping of Oscillations in Low-Prandtl-Number Convection.” <i>Journal of Fluid Mechanics</i>. Cambridge University Press, 2005. <a href=\"https://doi.org/10.1017/S0022112005006762\">https://doi.org/10.1017/S0022112005006762</a>.","ama":"Hof B, Juel A, Mullin T. Magnetohydrodynamic damping of oscillations in low-Prandtl-number convection. <i>Journal of Fluid Mechanics</i>. 2005;545:193-201. doi:<a href=\"https://doi.org/10.1017/S0022112005006762\">10.1017/S0022112005006762</a>","ista":"Hof B, Juel A, Mullin T. 2005. Magnetohydrodynamic damping of oscillations in low-Prandtl-number convection. Journal of Fluid Mechanics. 545, 193–201.","mla":"Hof, Björn, et al. “Magnetohydrodynamic Damping of Oscillations in Low-Prandtl-Number Convection.” <i>Journal of Fluid Mechanics</i>, vol. 545, Cambridge University Press, 2005, pp. 193–201, doi:<a href=\"https://doi.org/10.1017/S0022112005006762\">10.1017/S0022112005006762</a>.","short":"B. Hof, A. Juel, T. Mullin, Journal of Fluid Mechanics 545 (2005) 193–201."},"date_published":"2005-12-25T00:00:00Z","publisher":"Cambridge University Press","title":"Magnetohydrodynamic damping of oscillations in low-Prandtl-number convection","volume":545,"abstract":[{"text":"We present the results of an experimental investigation of the effect of a magnetic field on the stability of convection in a liquid metal. A rectangular container of gallium is subjected to a horizontal temperature gradient and a uniform magnetic field is applied separately in three directions. The magnetic field suppresses the oscillation most effectively when it is applied in the vertical direction and is least efficient when applied in the direction of the temperature gradient. The critical temperature difference required for the onset of oscillations is found to scale exponentially with the magnitude of the magnetic field for all three orientations. Comparisons are made with available theory and qualitative differences are discussed.","lang":"eng"}],"publication_status":"published","month":"12"},{"title":"Developmental specificity of auxin response by pairs of ARF and Aux/IAA transcriptional regulators","volume":24,"publisher":"Wiley-Blackwell","date_published":"2005-05-18T00:00:00Z","issue":"10","month":"05","publication_status":"published","abstract":[{"lang":"eng","text":"The plant hormone auxin elicits many specific context-dependent developmental responses. Auxin promotes degradation of Aux/IAA proteins that prevent transcription factors of the auxin response factor (ARF) family from regulating auxin-responsive target genes. Aux/IAAs and ARFs are represented by large gene families in Arabidopsis. Here we show that stabilization of BDL/IAA12 or its sister protein IAA13 prevents MP/ARF5-dependent embryonic root formation whereas stabilized SHY2/IAA3 interferes with seedling growth. Although both bdl and shy2-2 proteins inhibited MP/ARF5-dependent reporter gene activation, shy2-2 was much less efficient than bdl to interfere with embryonic root initiation when expressed from the BDL promoter. Similarly, MP was much more efficient than ARF16 in this process. When expressed from the SHY2 promoter, both shy2-2 and bdl inhibited cell elongation and auxin-induced gene expression in the seedling hypocotyl. By contrast, gravitropism and auxin-induced gene expression in the root, which were promoted by functionally redundant NPH4/ARF7 and ARF19 proteins, were inhibited by shy2-2, but not by bdl protein. Our results suggest that auxin signals are converted into specific responses by matching pairs of coexpressed ARF and Aux/IAA proteins."}],"author":[{"last_name":"Weijers","first_name":"Dolf","full_name":"Weijers, Dolf"},{"first_name":"Eva","last_name":"Benková","orcid":"0000-0002-8510-9739","id":"38F4F166-F248-11E8-B48F-1D18A9856A87","full_name":"Eva Benková"},{"first_name":"Katja","last_name":"Jäger","full_name":"Jäger, Katja E"},{"last_name":"Schlereth","first_name":"Alexandra","full_name":"Schlereth, Alexandra"},{"full_name":"Hamann, Thorsten","last_name":"Hamann","first_name":"Thorsten"},{"full_name":"Kientz, Marika","last_name":"Kientz","first_name":"Marika"},{"first_name":"Jill","last_name":"Wilmoth","full_name":"Wilmoth, Jill C"},{"last_name":"Reed","first_name":"Jason","full_name":"Reed, Jason W"},{"full_name":"Jürgens, Gerd","last_name":"Jürgens","first_name":"Gerd"}],"citation":{"short":"D. Weijers, E. Benková, K. Jäger, A. Schlereth, T. Hamann, M. Kientz, J. Wilmoth, J. Reed, G. Jürgens, EMBO Journal 24 (2005) 1874–1885.","mla":"Weijers, Dolf, et al. “Developmental Specificity of Auxin Response by Pairs of ARF and Aux/IAA Transcriptional Regulators.” <i>EMBO Journal</i>, vol. 24, no. 10, Wiley-Blackwell, 2005, pp. 1874–85, doi:<a href=\"https://doi.org/10.1038/sj.emboj.7600659\">10.1038/sj.emboj.7600659</a>.","ama":"Weijers D, Benková E, Jäger K, et al. Developmental specificity of auxin response by pairs of ARF and Aux/IAA transcriptional regulators. <i>EMBO Journal</i>. 2005;24(10):1874-1885. doi:<a href=\"https://doi.org/10.1038/sj.emboj.7600659\">10.1038/sj.emboj.7600659</a>","ista":"Weijers D, Benková E, Jäger K, Schlereth A, Hamann T, Kientz M, Wilmoth J, Reed J, Jürgens G. 2005. Developmental specificity of auxin response by pairs of ARF and Aux/IAA transcriptional regulators. EMBO Journal. 24(10), 1874–1885.","chicago":"Weijers, Dolf, Eva Benková, Katja Jäger, Alexandra Schlereth, Thorsten Hamann, Marika Kientz, Jill Wilmoth, Jason Reed, and Gerd Jürgens. “Developmental Specificity of Auxin Response by Pairs of ARF and Aux/IAA Transcriptional Regulators.” <i>EMBO Journal</i>. Wiley-Blackwell, 2005. <a href=\"https://doi.org/10.1038/sj.emboj.7600659\">https://doi.org/10.1038/sj.emboj.7600659</a>.","apa":"Weijers, D., Benková, E., Jäger, K., Schlereth, A., Hamann, T., Kientz, M., … Jürgens, G. (2005). Developmental specificity of auxin response by pairs of ARF and Aux/IAA transcriptional regulators. <i>EMBO Journal</i>. Wiley-Blackwell. <a href=\"https://doi.org/10.1038/sj.emboj.7600659\">https://doi.org/10.1038/sj.emboj.7600659</a>","ieee":"D. Weijers <i>et al.</i>, “Developmental specificity of auxin response by pairs of ARF and Aux/IAA transcriptional regulators,” <i>EMBO Journal</i>, vol. 24, no. 10. Wiley-Blackwell, pp. 1874–1885, 2005."},"extern":1,"quality_controlled":0,"date_updated":"2021-01-12T07:00:22Z","publication":"EMBO Journal","publist_id":"3918","intvolume":"        24","year":"2005","status":"public","day":"18","doi":"10.1038/sj.emboj.7600659","page":"1874 - 1885","main_file_link":[{"open_access":"1","url":"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1142592/"}],"_id":"2867","type":"journal_article","date_created":"2018-12-11T12:00:01Z","oa":1},{"author":[{"last_name":"Carneiro","first_name":"Jorge","full_name":"Carneiro, Jorge"},{"full_name":"Tiago Paixao","id":"2C5658E6-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2361-3953","first_name":"Tiago","last_name":"Paixao"},{"full_name":"Milutinovic, Dejan","first_name":"Dejan","last_name":"Milutinovic"},{"full_name":"Sousa, João","last_name":"Sousa","first_name":"João"},{"last_name":"Leon","first_name":"Kalet","full_name":"Leon, Kalet"},{"full_name":"Gardner, Rui","last_name":"Gardner","first_name":"Rui"},{"first_name":"Jose","last_name":"Faro","full_name":"Faro, Jose"}],"citation":{"apa":"Carneiro, J., Paixao, T., Milutinovic, D., Sousa, J., Leon, K., Gardner, R., &#38; Faro, J. (2005). Immunological self tolerance: Lessons from mathematical modeling. <i>Journal of Computational and Applied Mathematics</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.cam.2004.10.025\">https://doi.org/10.1016/j.cam.2004.10.025</a>","chicago":"Carneiro, Jorge, Tiago Paixao, Dejan Milutinovic, João Sousa, Kalet Leon, Rui Gardner, and Jose Faro. “Immunological Self Tolerance: Lessons from Mathematical Modeling.” <i>Journal of Computational and Applied Mathematics</i>. Elsevier, 2005. <a href=\"https://doi.org/10.1016/j.cam.2004.10.025\">https://doi.org/10.1016/j.cam.2004.10.025</a>.","ista":"Carneiro J, Paixao T, Milutinovic D, Sousa J, Leon K, Gardner R, Faro J. 2005. Immunological self tolerance: Lessons from mathematical modeling. Journal of Computational and Applied Mathematics. 184(1), 77–100.","ama":"Carneiro J, Paixao T, Milutinovic D, et al. Immunological self tolerance: Lessons from mathematical modeling. <i>Journal of Computational and Applied Mathematics</i>. 2005;184(1):77-100. doi:<a href=\"https://doi.org/10.1016/j.cam.2004.10.025\">10.1016/j.cam.2004.10.025</a>","ieee":"J. Carneiro <i>et al.</i>, “Immunological self tolerance: Lessons from mathematical modeling,” <i>Journal of Computational and Applied Mathematics</i>, vol. 184, no. 1. Elsevier, pp. 77–100, 2005.","short":"J. Carneiro, T. Paixao, D. Milutinovic, J. Sousa, K. Leon, R. Gardner, J. Faro, Journal of Computational and Applied Mathematics 184 (2005) 77–100.","mla":"Carneiro, Jorge, et al. “Immunological Self Tolerance: Lessons from Mathematical Modeling.” <i>Journal of Computational and Applied Mathematics</i>, vol. 184, no. 1, Elsevier, 2005, pp. 77–100, doi:<a href=\"https://doi.org/10.1016/j.cam.2004.10.025\">10.1016/j.cam.2004.10.025</a>."},"date_updated":"2021-01-12T07:00:32Z","extern":1,"quality_controlled":0,"title":"Immunological self tolerance: Lessons from mathematical modeling","volume":184,"publisher":"Elsevier","date_published":"2005-12-01T00:00:00Z","issue":"1","abstract":[{"text":"One of the fundamental properties of the immune system is its capacity to avoid autoimmune diseases. The mechanism underlying this process, known as self-tolerance, is hitherto unresolved but seems to involve the control of clonal expansion of autoreactive lymphocytes. This article reviews mathematical modeling of self-tolerance, addressing two specific hypotheses. The first hypothesis posits that self-tolerance is mediated by tuning of activation thresholds, which makes autoreactive T lymphocytes reversibly &quot;anergic&quot; and unable to proliferate. The second hypothesis posits that the proliferation of autoreactive T lymphocytes is instead controlled by specific regulatory T lymphocytes. Models representing the population dynamics of autoreactive T lymphocytes according to these two hypotheses were derived. For each model we identified how cell density affects tolerance, and predicted the corresponding phase spaces and bifurcations. We show that the simple induction of proliferative anergy, as modeled here, has a density dependence that is only partially compatible with adoptive transfers of tolerance, and that the models of tolerance mediated by specific regulatory T cells are closer to the observations.","lang":"eng"}],"publication_status":"published","month":"12","page":"77 - 100","year":"2005","day":"01","status":"public","doi":"10.1016/j.cam.2004.10.025","acknowledgement":"The work was financially supported by Fundação para a Ciência e Tecnologia: grants  P/BIA/10094/1998,  POCTI/36413/99,  and  POCTI/MGI/46477/2002; and fellowships to JF (Praxis/BCC/18972/98), JS (BD/13546/97), KL (SFRH/BPD+/1157/2002), DM (SFRH/BD/2960/2000) and TP (SFRH/BD/10550/2002).","_id":"2895","type":"journal_article","date_created":"2018-12-11T12:00:12Z","publication":"Journal of Computational and Applied Mathematics","intvolume":"       184","publist_id":"3863"},{"quality_controlled":"1","extern":"1","date_updated":"2021-01-12T07:40:22Z","citation":{"mla":"Dhonukshe, Pankaj, et al. “Cell Polarity, Auxin Transport and Cytoskeleton Mediated Division Planes: Who Comes First?” <i>Protoplasma</i>, vol. 226, no. 1–2, Springer, 2005, pp. 67–73, doi:<a href=\"https://doi.org/10.1007/s00709-005-0104-8\">10.1007/s00709-005-0104-8</a>.","short":"P. Dhonukshe, J. Kleine Vehn, J. Friml, Protoplasma 226 (2005) 67–73.","ieee":"P. Dhonukshe, J. Kleine Vehn, and J. Friml, “Cell polarity, auxin transport and cytoskeleton mediated division planes: Who comes first?,” <i>Protoplasma</i>, vol. 226, no. 1–2. Springer, pp. 67–73, 2005.","ista":"Dhonukshe P, Kleine Vehn J, Friml J. 2005. Cell polarity, auxin transport and cytoskeleton mediated division planes: Who comes first? Protoplasma. 226(1–2), 67–73.","ama":"Dhonukshe P, Kleine Vehn J, Friml J. Cell polarity, auxin transport and cytoskeleton mediated division planes: Who comes first? <i>Protoplasma</i>. 2005;226(1-2):67-73. doi:<a href=\"https://doi.org/10.1007/s00709-005-0104-8\">10.1007/s00709-005-0104-8</a>","chicago":"Dhonukshe, Pankaj, Jürgen Kleine Vehn, and Jiří Friml. “Cell Polarity, Auxin Transport and Cytoskeleton Mediated Division Planes: Who Comes First?” <i>Protoplasma</i>. Springer, 2005. <a href=\"https://doi.org/10.1007/s00709-005-0104-8\">https://doi.org/10.1007/s00709-005-0104-8</a>.","apa":"Dhonukshe, P., Kleine Vehn, J., &#38; Friml, J. (2005). Cell polarity, auxin transport and cytoskeleton mediated division planes: Who comes first? <i>Protoplasma</i>. Springer. <a href=\"https://doi.org/10.1007/s00709-005-0104-8\">https://doi.org/10.1007/s00709-005-0104-8</a>"},"oa_version":"None","author":[{"full_name":"Dhonukshe, Pankaj","last_name":"Dhonukshe","first_name":"Pankaj"},{"full_name":"Kleine Vehn, Jürgen","first_name":"Jürgen","last_name":"Kleine Vehn"},{"id":"4159519E-F248-11E8-B48F-1D18A9856A87","full_name":"Friml, Jirí","last_name":"Friml","first_name":"Jirí","orcid":"0000-0002-8302-7596"}],"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","publication_status":"published","month":"10","abstract":[{"lang":"eng","text":"In plants, cell polarity is an issue more recurring than in other systems, because plants, due to their adaptive and flexible development, often change cell polarity postembryonically according to intrinsic cues and demands of the environment. Recent findings on the directional movement of the plant signalling molecule auxin provide a unique connection between individual cell polarity and the establishment of polarity at the tissue, organ, and whole-plant levels. Decisions about the subcellular polar targeting of PIN auxin transport components determine the direction of auxin flow between cells and consequently mediate multiple developmental events. In addition, mutations or chemical interference with PIN-based auxin transport result in abnormal cell divisions. Thus, the complicated links between cell polarity establishment, auxin transport, cytoskeleton, and oriented cell divisions now begin to emerge. Here we review the available literature on the issues of cell polarity in both plants and animals to extend our understanding on the generation, maintenance, and transmission of cell polarity in plants."}],"issue":"1-2","publisher":"Springer","date_published":"2005-10-01T00:00:00Z","language":[{"iso":"eng"}],"volume":226,"title":"Cell polarity, auxin transport and cytoskeleton mediated division planes: Who comes first?","date_created":"2018-12-11T12:00:47Z","_id":"3000","type":"journal_article","page":"67 - 73","year":"2005","doi":"10.1007/s00709-005-0104-8","day":"01","status":"public","publist_id":"3701","intvolume":"       226","publication":"Protoplasma"},{"author":[{"last_name":"Paciorek","first_name":"Tomasz","full_name":"Paciorek, Tomasz"},{"first_name":"Eva","last_name":"Zažímalová","full_name":"Zažímalová, Eva"},{"full_name":"Ruthardt, Nadia","first_name":"Nadia","last_name":"Ruthardt"},{"last_name":"Petrášek","first_name":"Jan","full_name":"Petrášek, Jan"},{"first_name":"York","last_name":"Stierhof","full_name":"Stierhof, York-Dieter"},{"first_name":"Jürgen","last_name":"Kleine Vehn","full_name":"Kleine-Vehn, Jürgen"},{"full_name":"Morris, David A","first_name":"David","last_name":"Morris"},{"last_name":"Emans","first_name":"Neil","full_name":"Emans, Neil"},{"full_name":"Jürgens, Gerd","first_name":"Gerd","last_name":"Jürgens"},{"full_name":"Geldner, Niko","first_name":"Niko","last_name":"Geldner"},{"orcid":"0000-0002-8302-7596","first_name":"Jirí","last_name":"Friml","full_name":"Jirí Friml","id":"4159519E-F248-11E8-B48F-1D18A9856A87"}],"date_updated":"2021-01-12T07:40:23Z","extern":1,"quality_controlled":0,"citation":{"ama":"Paciorek T, Zažímalová E, Ruthardt N, et al. Auxin inhibits endocytosis and promotes its own efflux from cells. <i>Nature</i>. 2005;435(7046):1251-1256. doi:<a href=\"https://doi.org/10.1038/nature03633\">10.1038/nature03633</a>","ista":"Paciorek T, Zažímalová E, Ruthardt N, Petrášek J, Stierhof Y, Kleine Vehn J, Morris D, Emans N, Jürgens G, Geldner N, Friml J. 2005. Auxin inhibits endocytosis and promotes its own efflux from cells. Nature. 435(7046), 1251–1256.","chicago":"Paciorek, Tomasz, Eva Zažímalová, Nadia Ruthardt, Jan Petrášek, York Stierhof, Jürgen Kleine Vehn, David Morris, et al. “Auxin Inhibits Endocytosis and Promotes Its Own Efflux from Cells.” <i>Nature</i>. Nature Publishing Group, 2005. <a href=\"https://doi.org/10.1038/nature03633\">https://doi.org/10.1038/nature03633</a>.","apa":"Paciorek, T., Zažímalová, E., Ruthardt, N., Petrášek, J., Stierhof, Y., Kleine Vehn, J., … Friml, J. (2005). Auxin inhibits endocytosis and promotes its own efflux from cells. <i>Nature</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/nature03633\">https://doi.org/10.1038/nature03633</a>","ieee":"T. Paciorek <i>et al.</i>, “Auxin inhibits endocytosis and promotes its own efflux from cells,” <i>Nature</i>, vol. 435, no. 7046. Nature Publishing Group, pp. 1251–1256, 2005.","mla":"Paciorek, Tomasz, et al. “Auxin Inhibits Endocytosis and Promotes Its Own Efflux from Cells.” <i>Nature</i>, vol. 435, no. 7046, Nature Publishing Group, 2005, pp. 1251–56, doi:<a href=\"https://doi.org/10.1038/nature03633\">10.1038/nature03633</a>.","short":"T. Paciorek, E. Zažímalová, N. Ruthardt, J. Petrášek, Y. Stierhof, J. Kleine Vehn, D. Morris, N. Emans, G. Jürgens, N. Geldner, J. Friml, Nature 435 (2005) 1251–1256."},"publisher":"Nature Publishing Group","date_published":"2005-06-30T00:00:00Z","volume":435,"title":"Auxin inhibits endocytosis and promotes its own efflux from cells","abstract":[{"text":"One of the mechanisms by which signalling molecules regulate cellular behaviour is modulating subcellular protein translocation. This mode of regulation is often based on specialized vesicle trafficking, termed constitutive cycling, which consists of repeated internalization and recycling of proteins to and from the plasma membrane. No such mechanism of hormone action has been shown in plants although several proteins, including the PIN auxin efflux facilitators, exhibit constitutive cycling. Here we show that a major regulator of plant development, auxin, inhibits endocytosis. This effect is specific to biologically active auxins and requires activity of the Calossin-like protein BIG. By inhibiting the internalization step of PIN constitutive cycling, auxin increases levels of PINs at the plasma membrane. Concomitantly, auxin promotes its own efflux from cells by a vesicle-trafficking-dependent mechanism. Furthermore, asymmetric auxin translocation during gravitropism is correlated with decreased PIN internalization. Our data imply a previously undescribed mode of plant hormone action: by modulating PIN protein trafficking, auxin regulates PIN abundance and activity at the cell surface, providing a mechanism for the feedback regulation of auxin transport.","lang":"eng"}],"publication_status":"published","month":"06","issue":"7046","page":"1251 - 1256","doi":"10.1038/nature03633","year":"2005","status":"public","day":"30","date_created":"2018-12-11T12:00:47Z","_id":"3001","type":"journal_article","intvolume":"       435","publist_id":"3702","publication":"Nature"},{"year":"2005","page":"4521 - 4531","doi":"10.1242/dev.02027","status":"public","day":"01","date_created":"2018-12-11T12:00:48Z","type":"journal_article","_id":"3003","publist_id":"3700","intvolume":"       132","publication":"Development","author":[{"last_name":"Vieten","first_name":"Anne","full_name":"Vieten, Anne"},{"full_name":"Vanneste, Steffen","last_name":"Vanneste","first_name":"Steffen"},{"full_name":"Wiśniewska, Justyna","last_name":"Wiśniewska","first_name":"Justyna"},{"id":"38F4F166-F248-11E8-B48F-1D18A9856A87","full_name":"Eva Benková","last_name":"Benková","first_name":"Eva","orcid":"0000-0002-8510-9739"},{"full_name":"Benjamins, René","first_name":"René","last_name":"Benjamins"},{"full_name":"Beeckman, Tom","last_name":"Beeckman","first_name":"Tom"},{"first_name":"Christian","last_name":"Luschnig","full_name":"Luschnig, Christian"},{"full_name":"Jirí Friml","id":"4159519E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-8302-7596","last_name":"Friml","first_name":"Jirí"}],"quality_controlled":0,"extern":1,"date_updated":"2021-01-12T07:40:23Z","citation":{"ieee":"A. Vieten <i>et al.</i>, “Functional redundancy of PIN proteins is accompanied by auxin-dependent cross-regulation of PIN expression,” <i>Development</i>, vol. 132, no. 20. Company of Biologists, pp. 4521–4531, 2005.","ama":"Vieten A, Vanneste S, Wiśniewska J, et al. Functional redundancy of PIN proteins is accompanied by auxin-dependent cross-regulation of PIN expression. <i>Development</i>. 2005;132(20):4521-4531. doi:<a href=\"https://doi.org/10.1242/dev.02027\">10.1242/dev.02027</a>","ista":"Vieten A, Vanneste S, Wiśniewska J, Benková E, Benjamins R, Beeckman T, Luschnig C, Friml J. 2005. Functional redundancy of PIN proteins is accompanied by auxin-dependent cross-regulation of PIN expression. Development. 132(20), 4521–4531.","chicago":"Vieten, Anne, Steffen Vanneste, Justyna Wiśniewska, Eva Benková, René Benjamins, Tom Beeckman, Christian Luschnig, and Jiří Friml. “Functional Redundancy of PIN Proteins Is Accompanied by Auxin-Dependent Cross-Regulation of PIN Expression.” <i>Development</i>. Company of Biologists, 2005. <a href=\"https://doi.org/10.1242/dev.02027\">https://doi.org/10.1242/dev.02027</a>.","apa":"Vieten, A., Vanneste, S., Wiśniewska, J., Benková, E., Benjamins, R., Beeckman, T., … Friml, J. (2005). Functional redundancy of PIN proteins is accompanied by auxin-dependent cross-regulation of PIN expression. <i>Development</i>. Company of Biologists. <a href=\"https://doi.org/10.1242/dev.02027\">https://doi.org/10.1242/dev.02027</a>","short":"A. Vieten, S. Vanneste, J. Wiśniewska, E. Benková, R. Benjamins, T. Beeckman, C. Luschnig, J. Friml, Development 132 (2005) 4521–4531.","mla":"Vieten, Anne, et al. “Functional Redundancy of PIN Proteins Is Accompanied by Auxin-Dependent Cross-Regulation of PIN Expression.” <i>Development</i>, vol. 132, no. 20, Company of Biologists, 2005, pp. 4521–31, doi:<a href=\"https://doi.org/10.1242/dev.02027\">10.1242/dev.02027</a>."},"date_published":"2005-10-01T00:00:00Z","publisher":"Company of Biologists","volume":132,"title":"Functional redundancy of PIN proteins is accompanied by auxin-dependent cross-regulation of PIN expression","month":"10","publication_status":"published","abstract":[{"text":"Plant development displays an exceptional plasticity and adaptability that involves the dynamic, asymmetric distribution of the phytohormone auxin. Polar auxin flow, which requires polarly localized transport facilitators of the PIN family, largely contributes to the establishment and maintenance of the auxin gradients. Functionally overlapping action of PIN proteins mediates multiple developmental processes, including embryo formation, organ development and tropisms. Here we show that PIN proteins exhibit synergistic interactions, which involve cross-regulation of PIN gene expression in pin mutants or plants with inhibited auxin transport. Auxin itself positively feeds back on PIN gene expression in a tissue-specific manner through an AUX/IAA-dependent signalling pathway. This regulatory switch is indicative of a mechanism by which the loss of a specific PIN protein is compensated for by auxin-dependent ectopic: expression of its homologues. The compensatory properties of the PIN-dependent transport network might enable the stabilization of auxin gradients and potentially contribute to the robustness of plant adaptive development.","lang":"eng"}],"issue":"20"},{"publication_status":"published","month":"07","abstract":[{"text":"Molecular mechanisms of pattern formation in the plant embryo are not well understood. Recent molecular and cellular studies, in conjunction with earlier microsurgical, physiological, and genetic work, are now starting to define the outlines of a model where gradients of the signaling molecule auxin play a central role in embryo patterning. It is relatively clear how these gradients are established and interpreted, but how they are maintained is still unresolved. Here, we have studied the contributions of auxin biosynthesis, conjugation, and transport pathways to the maintenance of embryonic auxin gradients. Auxin homeostasis in the embryo was manipulated by region-specific conditional expression of indoleacetic acid-tryptophan monooxygenase or indoleacetic acid-lysine synthetase, bacterial enzymes for auxin biosynthesis or conjugation. Neither manipulation of auxin biosynthesis nor of auxin conjugation interfered with auxin gradients and patterning in the embryo. This result suggests a compensatory mechanism for buffering auxin gradients in the embryo. Chemical and genetic inhibition revealed that auxin transport activity, in particular that of the PIN-FORMED1 (PIN1) and PIN4 proteins, is a major factor in the maintenance of these gradients.","lang":"eng"}],"issue":"9","date_published":"2005-07-01T00:00:00Z","publisher":"American Society of Plant Biologists","title":"Maintenance of embryonic auxin distribution for apical basal patterning by PIN FORMED dependent auxin transport in Arabidopsis","volume":17,"quality_controlled":0,"extern":1,"date_updated":"2021-01-12T07:40:24Z","citation":{"mla":"Weijers, Dolf, et al. “Maintenance of Embryonic Auxin Distribution for Apical Basal Patterning by PIN FORMED Dependent Auxin Transport in Arabidopsis.” <i>Plant Cell</i>, vol. 17, no. 9, American Society of Plant Biologists, 2005, pp. 2517–26, doi:<a href=\"https://doi.org/10.1105/tpc.105.034637\">10.1105/tpc.105.034637</a>.","short":"D. Weijers, M. Sauer, O. Meurette, J. Friml, K. Ljung, G. Sandberg, P. Hooykaas, R. Offringa, Plant Cell 17 (2005) 2517–2526.","chicago":"Weijers, Dolf, Michael Sauer, Olivier Meurette, Jiří Friml, Karin Ljung, Göran Sandberg, Paul Hooykaas, and Remko Offringa. “Maintenance of Embryonic Auxin Distribution for Apical Basal Patterning by PIN FORMED Dependent Auxin Transport in Arabidopsis.” <i>Plant Cell</i>. American Society of Plant Biologists, 2005. <a href=\"https://doi.org/10.1105/tpc.105.034637\">https://doi.org/10.1105/tpc.105.034637</a>.","ama":"Weijers D, Sauer M, Meurette O, et al. Maintenance of embryonic auxin distribution for apical basal patterning by PIN FORMED dependent auxin transport in Arabidopsis. <i>Plant Cell</i>. 2005;17(9):2517-2526. doi:<a href=\"https://doi.org/10.1105/tpc.105.034637\">10.1105/tpc.105.034637</a>","ista":"Weijers D, Sauer M, Meurette O, Friml J, Ljung K, Sandberg G, Hooykaas P, Offringa R. 2005. Maintenance of embryonic auxin distribution for apical basal patterning by PIN FORMED dependent auxin transport in Arabidopsis. Plant Cell. 17(9), 2517–2526.","apa":"Weijers, D., Sauer, M., Meurette, O., Friml, J., Ljung, K., Sandberg, G., … Offringa, R. (2005). Maintenance of embryonic auxin distribution for apical basal patterning by PIN FORMED dependent auxin transport in Arabidopsis. <i>Plant Cell</i>. American Society of Plant Biologists. <a href=\"https://doi.org/10.1105/tpc.105.034637\">https://doi.org/10.1105/tpc.105.034637</a>","ieee":"D. Weijers <i>et al.</i>, “Maintenance of embryonic auxin distribution for apical basal patterning by PIN FORMED dependent auxin transport in Arabidopsis,” <i>Plant Cell</i>, vol. 17, no. 9. American Society of Plant Biologists, pp. 2517–2526, 2005."},"author":[{"last_name":"Weijers","first_name":"Dolf","full_name":"Weijers, Dolf"},{"full_name":"Sauer, Michael","last_name":"Sauer","first_name":"Michael"},{"full_name":"Meurette, Olivier","last_name":"Meurette","first_name":"Olivier"},{"full_name":"Jirí Friml","id":"4159519E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-8302-7596","last_name":"Friml","first_name":"Jirí"},{"full_name":"Ljung, Karin","last_name":"Ljung","first_name":"Karin"},{"last_name":"Sandberg","first_name":"Göran","full_name":"Sandberg, Göran"},{"full_name":"Hooykaas, Paul","last_name":"Hooykaas","first_name":"Paul"},{"last_name":"Offringa","first_name":"Remko","full_name":"Offringa, Remko"}],"publist_id":"3698","intvolume":"        17","publication":"Plant Cell","date_created":"2018-12-11T12:00:48Z","_id":"3004","type":"journal_article","year":"2005","day":"01","status":"public","page":"2517 - 2526","doi":"10.1105/tpc.105.034637"},{"page":"26 - 31","doi":"10.1038/nsmb870","day":"01","year":"2005","status":"public","date_created":"2018-12-11T12:01:38Z","type":"journal_article","_id":"3141","intvolume":"        12","publist_id":"3554","publication":"Nature Structural and Molecular Biology","author":[{"last_name":"Rodal","first_name":"Avital","full_name":"Rodal, Avital A"},{"last_name":"Sokolova","first_name":"Olga","full_name":"Sokolova, Olga"},{"last_name":"Robins","first_name":"Deborah","full_name":"Robins, Deborah B"},{"last_name":"Daugherty","first_name":"Karen","full_name":"Daugherty, Karen M"},{"full_name":"Simon Hippenmeyer","id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061","first_name":"Simon","last_name":"Hippenmeyer"},{"first_name":"Howard","last_name":"Riezman","full_name":"Riezman, Howard"},{"last_name":"Grigorieff","first_name":"Nikolaus","full_name":"Grigorieff, Nikolaus"},{"last_name":"Goode","first_name":"Bruce","full_name":"Goode, Bruce L"}],"date_updated":"2021-01-12T07:41:21Z","quality_controlled":0,"extern":1,"citation":{"short":"A. Rodal, O. Sokolova, D. Robins, K. Daugherty, S. Hippenmeyer, H. Riezman, N. Grigorieff, B. Goode, Nature Structural and Molecular Biology 12 (2005) 26–31.","mla":"Rodal, Avital, et al. “Conformational Changes in the Arp2 3 Complex Leading to Actin Nucleation.” <i>Nature Structural and Molecular Biology</i>, vol. 12, no. 1, Nature Publishing Group, 2005, pp. 26–31, doi:<a href=\"https://doi.org/10.1038/nsmb870\">10.1038/nsmb870</a>.","apa":"Rodal, A., Sokolova, O., Robins, D., Daugherty, K., Hippenmeyer, S., Riezman, H., … Goode, B. (2005). Conformational changes in the Arp2 3 complex leading to actin nucleation. <i>Nature Structural and Molecular Biology</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/nsmb870\">https://doi.org/10.1038/nsmb870</a>","ama":"Rodal A, Sokolova O, Robins D, et al. Conformational changes in the Arp2 3 complex leading to actin nucleation. <i>Nature Structural and Molecular Biology</i>. 2005;12(1):26-31. doi:<a href=\"https://doi.org/10.1038/nsmb870\">10.1038/nsmb870</a>","ista":"Rodal A, Sokolova O, Robins D, Daugherty K, Hippenmeyer S, Riezman H, Grigorieff N, Goode B. 2005. Conformational changes in the Arp2 3 complex leading to actin nucleation. Nature Structural and Molecular Biology. 12(1), 26–31.","chicago":"Rodal, Avital, Olga Sokolova, Deborah Robins, Karen Daugherty, Simon Hippenmeyer, Howard Riezman, Nikolaus Grigorieff, and Bruce Goode. “Conformational Changes in the Arp2 3 Complex Leading to Actin Nucleation.” <i>Nature Structural and Molecular Biology</i>. Nature Publishing Group, 2005. <a href=\"https://doi.org/10.1038/nsmb870\">https://doi.org/10.1038/nsmb870</a>.","ieee":"A. Rodal <i>et al.</i>, “Conformational changes in the Arp2 3 complex leading to actin nucleation,” <i>Nature Structural and Molecular Biology</i>, vol. 12, no. 1. Nature Publishing Group, pp. 26–31, 2005."},"publisher":"Nature Publishing Group","date_published":"2005-01-01T00:00:00Z","title":"Conformational changes in the Arp2 3 complex leading to actin nucleation","volume":12,"abstract":[{"lang":"eng","text":"The two actin-related subunits of the Arp2/3 complex, Arp2 and Arp3, are proposed to form a pseudo actin dimer that nucleates actin polymerization. However, in the crystal structure of the inactive complex, they are too far apart to form such a nucleus. Here, we show using EM that yeast and bovine Arp2/3 complexes exist in a distribution among open, intermediate and closed conformations. The crystal structure docks well into the open conformation. The activator WASp binds at the cleft between Arp2 and Arp3, and all WASp-bound complexes are closed. The inhibitor coronin binds near the p35 subunit, and all coronin-bound complexes are open. Activating and loss-of-function mutations in the p35 subunit skew conformational distribution in opposite directions, closed and open, respectively. We conclude that WASp stabilizes p35-dependent closure of the complex, holding Arp2 and Arp3 closer together to nucleate an actin filament."}],"publication_status":"published","month":"01","issue":"1"},{"publist_id":"3552","intvolume":"         3","publication":"PLoS Biology","date_created":"2018-12-11T12:01:38Z","_id":"3143","type":"journal_article","doi":"10.1371/journal.pbio.0030159","license":"https://creativecommons.org/licenses/by/4.0/","page":"0878 - 0890","year":"2005","status":"public","day":"01","publication_status":"published","month":"05","abstract":[{"lang":"eng","text":"Two ETS transcription factors of the Pea3 subfamily are induced in subpopulations of dorsal root ganglion (DRG) sensory and spinal motor neurons by target-derived factors. Their expression controls late aspects of neuronal differentiation such as target invasion and branching. Here, we show that the late onset of ETS gene expression is an essential requirement for normal sensory neuron differentiation. We provide genetic evidence in the mouse that precocious ETS expression in DRG sensory neurons perturbs axonal projections, the acquisition of terminal differentiation markers, and their dependence on neurotrophic support. Together, our findings indicate that DRG sensory neurons exhibit a temporal developmental switch that can be revealed by distinct responses to ETS transcription factor signaling at sequential steps of neuronal maturation."}],"issue":"5","publisher":"Public Library of Science","date_published":"2005-05-01T00:00:00Z","title":"A developmental switch in the response of DRG neurons to ETS transcription factor signaling","volume":3,"quality_controlled":0,"extern":1,"date_updated":"2021-01-12T07:41:21Z","citation":{"ama":"Hippenmeyer S, Vrieseling E, Sigrist M, et al. A developmental switch in the response of DRG neurons to ETS transcription factor signaling. <i>PLoS Biology</i>. 2005;3(5):0878-0890. doi:<a href=\"https://doi.org/10.1371/journal.pbio.0030159\">10.1371/journal.pbio.0030159</a>","chicago":"Hippenmeyer, Simon, Eline Vrieseling, Markus Sigrist, Thomas Portmann, Celia Laengle, David Ladle, and Silvia Arber. “A Developmental Switch in the Response of DRG Neurons to ETS Transcription Factor Signaling.” <i>PLoS Biology</i>. Public Library of Science, 2005. <a href=\"https://doi.org/10.1371/journal.pbio.0030159\">https://doi.org/10.1371/journal.pbio.0030159</a>.","ista":"Hippenmeyer S, Vrieseling E, Sigrist M, Portmann T, Laengle C, Ladle D, Arber S. 2005. A developmental switch in the response of DRG neurons to ETS transcription factor signaling. PLoS Biology. 3(5), 0878–0890.","apa":"Hippenmeyer, S., Vrieseling, E., Sigrist, M., Portmann, T., Laengle, C., Ladle, D., &#38; Arber, S. (2005). A developmental switch in the response of DRG neurons to ETS transcription factor signaling. <i>PLoS Biology</i>. Public Library of Science. <a href=\"https://doi.org/10.1371/journal.pbio.0030159\">https://doi.org/10.1371/journal.pbio.0030159</a>","ieee":"S. Hippenmeyer <i>et al.</i>, “A developmental switch in the response of DRG neurons to ETS transcription factor signaling,” <i>PLoS Biology</i>, vol. 3, no. 5. Public Library of Science, pp. 0878–0890, 2005.","short":"S. Hippenmeyer, E. Vrieseling, M. Sigrist, T. Portmann, C. Laengle, D. Ladle, S. Arber, PLoS Biology 3 (2005) 0878–0890.","mla":"Hippenmeyer, Simon, et al. “A Developmental Switch in the Response of DRG Neurons to ETS Transcription Factor Signaling.” <i>PLoS Biology</i>, vol. 3, no. 5, Public Library of Science, 2005, pp. 0878–90, doi:<a href=\"https://doi.org/10.1371/journal.pbio.0030159\">10.1371/journal.pbio.0030159</a>."},"author":[{"full_name":"Simon Hippenmeyer","id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer","first_name":"Simon"},{"last_name":"Vrieseling","first_name":"Eline","full_name":"Vrieseling, Eline"},{"full_name":"Sigrist, Markus","first_name":"Markus","last_name":"Sigrist"},{"full_name":"Portmann, Thomas","first_name":"Thomas","last_name":"Portmann"},{"last_name":"Laengle","first_name":"Celia","full_name":"Laengle, Celia"},{"first_name":"David","last_name":"Ladle","full_name":"Ladle, David R"},{"first_name":"Silvia","last_name":"Arber","full_name":"Arber, Silvia"}],"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)"}}]