[{"article_type":"original","year":"2003","oa_version":"Published Version","scopus_import":"1","external_id":{"pmid":["12705868"]},"date_updated":"2022-07-18T08:57:42Z","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","publication_identifier":{"issn":["0092-8674"]},"article_processing_charge":"No","issue":"2","_id":"11122","abstract":[{"lang":"eng","text":"Nuclear pore complexes (NPCs) are large multiprotein assemblies that allow traffic between the cytoplasm and the nucleus. During mitosis in higher eukaryotes, the Nuclear Envelope (NE) breaks down and NPCs disassemble. How NPCs reassemble and incorporate into the NE upon mitotic exit is poorly understood. We demonstrate a function for the conserved Nup107-160 complex in this process. Partial in vivo depletion of Nup133 or Nup107 via RNAi in HeLa cells resulted in reduced levels of multiple nucleoporins and decreased NPC density in the NE. Immunodepletion of the entire Nup107-160 complex from in vitro nuclear assembly reactions produced nuclei with a continuous NE but no NPCs. This phenotype was reversible only if Nup107-160 complex was readded before closed NE formation. Depletion also prevented association of FG-repeat nucleoporins with chromatin. We propose a stepwise model in which postmitotic NPC assembly initiates on chromatin via early recruitment of the Nup107-160 complex."}],"date_published":"2003-04-17T00:00:00Z","publication_status":"published","volume":113,"citation":{"short":"T.C. Walther, A. Alves, H. Pickersgill, I. Loı̈odice, M. Hetzer, V. Galy, B.B. Hülsmann, T. Köcher, M. Wilm, T. Allen, I.W. Mattaj, V. Doye, Cell 113 (2003) 195–206.","ama":"Walther TC, Alves A, Pickersgill H, et al. The conserved Nup107-160 complex is critical for nuclear pore complex assembly. <i>Cell</i>. 2003;113(2):195-206. doi:<a href=\"https://doi.org/10.1016/s0092-8674(03)00235-6\">10.1016/s0092-8674(03)00235-6</a>","apa":"Walther, T. C., Alves, A., Pickersgill, H., Loı̈odice, I., Hetzer, M., Galy, V., … Doye, V. (2003). The conserved Nup107-160 complex is critical for nuclear pore complex assembly. <i>Cell</i>. Elsevier. <a href=\"https://doi.org/10.1016/s0092-8674(03)00235-6\">https://doi.org/10.1016/s0092-8674(03)00235-6</a>","chicago":"Walther, Tobias C., Annabelle Alves, Helen Pickersgill, Isabelle Loı̈odice, Martin Hetzer, Vincent Galy, Bastian B. Hülsmann, et al. “The Conserved Nup107-160 Complex Is Critical for Nuclear Pore Complex Assembly.” <i>Cell</i>. Elsevier, 2003. <a href=\"https://doi.org/10.1016/s0092-8674(03)00235-6\">https://doi.org/10.1016/s0092-8674(03)00235-6</a>.","ista":"Walther TC, Alves A, Pickersgill H, Loı̈odice I, Hetzer M, Galy V, Hülsmann BB, Köcher T, Wilm M, Allen T, Mattaj IW, Doye V. 2003. The conserved Nup107-160 complex is critical for nuclear pore complex assembly. Cell. 113(2), 195–206.","ieee":"T. C. Walther <i>et al.</i>, “The conserved Nup107-160 complex is critical for nuclear pore complex assembly,” <i>Cell</i>, vol. 113, no. 2. Elsevier, pp. 195–206, 2003.","mla":"Walther, Tobias C., et al. “The Conserved Nup107-160 Complex Is Critical for Nuclear Pore Complex Assembly.” <i>Cell</i>, vol. 113, no. 2, Elsevier, 2003, pp. 195–206, doi:<a href=\"https://doi.org/10.1016/s0092-8674(03)00235-6\">10.1016/s0092-8674(03)00235-6</a>."},"title":"The conserved Nup107-160 complex is critical for nuclear pore complex assembly","day":"17","author":[{"last_name":"Walther","first_name":"Tobias C.","full_name":"Walther, Tobias C."},{"last_name":"Alves","full_name":"Alves, Annabelle","first_name":"Annabelle"},{"last_name":"Pickersgill","first_name":"Helen","full_name":"Pickersgill, Helen"},{"last_name":"Loı̈odice","full_name":"Loı̈odice, Isabelle","first_name":"Isabelle"},{"id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","orcid":"0000-0002-2111-992X","first_name":"Martin W","full_name":"HETZER, Martin W","last_name":"HETZER"},{"full_name":"Galy, Vincent","first_name":"Vincent","last_name":"Galy"},{"first_name":"Bastian B.","full_name":"Hülsmann, Bastian B.","last_name":"Hülsmann"},{"last_name":"Köcher","full_name":"Köcher, Thomas","first_name":"Thomas"},{"first_name":"Matthias","full_name":"Wilm, Matthias","last_name":"Wilm"},{"last_name":"Allen","full_name":"Allen, Terry","first_name":"Terry"},{"first_name":"Iain W.","full_name":"Mattaj, Iain W.","last_name":"Mattaj"},{"first_name":"Valérie","full_name":"Doye, Valérie","last_name":"Doye"}],"type":"journal_article","pmid":1,"keyword":["General Biochemistry","Genetics and Molecular Biology"],"language":[{"iso":"eng"}],"doi":"10.1016/s0092-8674(03)00235-6","page":"195-206","month":"04","extern":"1","date_created":"2022-04-07T07:57:10Z","publisher":"Elsevier","publication":"Cell","quality_controlled":"1","status":"public","intvolume":"       113"},{"article_processing_charge":"No","issue":"5","date_published":"2002-03-08T00:00:00Z","_id":"2989","abstract":[{"text":"In contrast to animals, little is known about pattern formation in plants. Physiological and genetic data suggest the involvement of the phytohormone auxin in this process. Here, we characterize a novel member of the PIN family of putative auxin efflux carriers, Arabidopsis PIN4, that is localized in developing and mature root meristems. Atpin4 mutants are defective in establishment and maintenance of endogenous auxin gradients, fail to canalize externally applied auxin, and display various patterning defects in both embryonic and seedling roots. We propose a role for AtPIN4 in generating a sink for auxin below the quiescent center of the root meristem that is essential for auxin distribution and patterning.","lang":"eng"}],"publication_status":"published","volume":108,"article_type":"original","publist_id":"3713","year":"2002","oa_version":"None","scopus_import":"1","external_id":{"pmid":["11893337"]},"date_updated":"2023-07-17T11:57:40Z","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","publication_identifier":{"issn":["0092-8674"]},"page":"661 - 673","month":"03","extern":"1","date_created":"2018-12-11T12:00:43Z","publisher":"Cell Press","publication":"Cell","quality_controlled":"1","intvolume":"       108","status":"public","citation":{"chicago":"Friml, Jiří, Eva Benková, Ikram Blilou, Justyna Wiśniewska, Thorsten Hamann, Karin Ljung, Scott Woody, et al. “AtPIN4 Mediates Sink-Driven Auxin Gradients and Root Patterning in Arabidopsis.” <i>Cell</i>. Cell Press, 2002. <a href=\"https://doi.org/10.1016/S0092-8674(02)00656-6\">https://doi.org/10.1016/S0092-8674(02)00656-6</a>.","ista":"Friml J, Benková E, Blilou I, Wiśniewska J, Hamann T, Ljung K, Woody S, Sandberg G, Scheres B, Jürgens G, Palme K. 2002. AtPIN4 mediates sink-driven auxin gradients and root patterning in Arabidopsis. Cell. 108(5), 661–673.","ieee":"J. Friml <i>et al.</i>, “AtPIN4 mediates sink-driven auxin gradients and root patterning in Arabidopsis,” <i>Cell</i>, vol. 108, no. 5. Cell Press, pp. 661–673, 2002.","mla":"Friml, Jiří, et al. “AtPIN4 Mediates Sink-Driven Auxin Gradients and Root Patterning in Arabidopsis.” <i>Cell</i>, vol. 108, no. 5, Cell Press, 2002, pp. 661–73, doi:<a href=\"https://doi.org/10.1016/S0092-8674(02)00656-6\">10.1016/S0092-8674(02)00656-6</a>.","short":"J. Friml, E. Benková, I. Blilou, J. Wiśniewska, T. Hamann, K. Ljung, S. Woody, G. Sandberg, B. Scheres, G. Jürgens, K. Palme, Cell 108 (2002) 661–673.","ama":"Friml J, Benková E, Blilou I, et al. AtPIN4 mediates sink-driven auxin gradients and root patterning in Arabidopsis. <i>Cell</i>. 2002;108(5):661-673. doi:<a href=\"https://doi.org/10.1016/S0092-8674(02)00656-6\">10.1016/S0092-8674(02)00656-6</a>","apa":"Friml, J., Benková, E., Blilou, I., Wiśniewska, J., Hamann, T., Ljung, K., … Palme, K. (2002). AtPIN4 mediates sink-driven auxin gradients and root patterning in Arabidopsis. <i>Cell</i>. Cell Press. <a href=\"https://doi.org/10.1016/S0092-8674(02)00656-6\">https://doi.org/10.1016/S0092-8674(02)00656-6</a>"},"title":"AtPIN4 mediates sink-driven auxin gradients and root patterning in Arabidopsis","day":"08","type":"journal_article","author":[{"last_name":"Friml","full_name":"Friml, Jirí","first_name":"Jirí","id":"4159519E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-8302-7596"},{"last_name":"Benková","full_name":"Benková, Eva","first_name":"Eva","id":"38F4F166-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-8510-9739"},{"first_name":"Ikram","full_name":"Blilou, Ikram","last_name":"Blilou"},{"last_name":"Wiśniewska","first_name":"Justyna","full_name":"Wiśniewska, Justyna"},{"last_name":"Hamann","full_name":"Hamann, Thorsten","first_name":"Thorsten"},{"first_name":"Karin","full_name":"Ljung, Karin","last_name":"Ljung"},{"full_name":"Woody, Scott","first_name":"Scott","last_name":"Woody"},{"last_name":"Sandberg","full_name":"Sandberg, Göran","first_name":"Göran"},{"last_name":"Scheres","full_name":"Scheres, Ben","first_name":"Ben"},{"last_name":"Jürgens","full_name":"Jürgens, Gerd","first_name":"Gerd"},{"last_name":"Palme","full_name":"Palme, Klaus","first_name":"Klaus"}],"pmid":1,"acknowledgement":"We thank Petra Tänzler, Michaela Lehnen, and Thomas Steinmann for technical help. We acknowledge the Arabidopsis Biological Resource Center (Columbus, OH) and Thomas Altman for providing material. We also gratefully acknowledge the ADIS service group for DNA sequencing and ZIGIA (Center for Functional Genomics in Arabidopsis) for the En lines. We are grateful to our colleagues, particularly Leo Gälweiler, Niko Geldner, Matthias Godde, and Kathrin Schrick for critical reading of the manuscript. This work was supported by a fellowship of the Deutscher Akademischer Austauschdienset (J.F.), the Deutsche Forschungsgemeinschaft (Schwerpunktprogramm Phytohormone), the European Communities Biotechnology Programs, the Fonds der Chemischen Industrie, and the INCO-Copernicus Program.","language":[{"iso":"eng"}],"doi":"10.1016/S0092-8674(02)00656-6"},{"publication_identifier":{"issn":["0092-8674"]},"external_id":{"pmid":["9778244 "]},"scopus_import":"1","date_updated":"2022-08-31T13:46:20Z","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","oa_version":"None","year":"1998","article_type":"original","publist_id":"4312","volume":95,"publication_status":"published","date_published":"1998-10-02T00:00:00Z","_id":"2586","abstract":[{"lang":"eng","text":"The role of inhibitory Golgi cells in cerebellar function was investigated by selectively ablating Golgi cells expressing human interleukin-2 receptor α subunit in transgenic mice, using the immunotoxin- mediated cell targeting technique. Golgi cell disruption caused severe acute motor disorders. These mice showed gradual recovery but retained a continuing inability to perform compound movements. Optical and electrical recordings combined with immunocytological analysis indicated that elimination of Golgi cells not only reduces GABA-mediated inhibition but also attenuates functional NMDA receptors in granule cells. These results demonstrate that synaptic integration involving both GABA inhibition and NMDA receptor activation is essential for compound motor coordination. Furthermore, this integration can adapt after Golgi cell elimination so as not to evoke overexcitation by the reduction of NMDA receptors."}],"article_processing_charge":"No","issue":"1","doi":"10.1016/S0092-8674(00)81779-1","language":[{"iso":"eng"}],"pmid":1,"acknowledgement":"We thank Kumlesh K Dev for careful reading of this manuscript, Peter Somogyi and Hirohide Sawada for invaluable advice, and Akira Uesugi for photographic assistance. This work was supported in part by research grants from the Ministry of Education, Science and Culture of Japan. the Sankyo Foundation. the Yamanouchi Founda-tion. the Biomolecular Engineering Research Institute, CREST and the International Resource Program of the National Cancer Institute. \r\n","author":[{"full_name":"Watanabe, Dai","first_name":"Dai","last_name":"Watanabe"},{"last_name":"Inokawa","first_name":"Hitoshi","full_name":"Inokawa, Hitoshi"},{"full_name":"Hashimoto, Kouichi","first_name":"Kouichi","last_name":"Hashimoto"},{"first_name":"Noboru","full_name":"Suzuki, Noboru","last_name":"Suzuki"},{"last_name":"Kano","full_name":"Kano, Masanobu","first_name":"Masanobu"},{"orcid":"0000-0001-8761-9444","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","first_name":"Ryuichi","full_name":"Shigemoto, Ryuichi","last_name":"Shigemoto"},{"full_name":"Hirano, Tomoo","first_name":"Tomoo","last_name":"Hirano"},{"first_name":"Keisuke","full_name":"Toyama, Keisuke","last_name":"Toyama"},{"full_name":"Kaneko, Satoshi","first_name":"Satoshi","last_name":"Kaneko"},{"last_name":"Yokoi","first_name":"Mineto","full_name":"Yokoi, Mineto"},{"last_name":"Moriyoshi","full_name":"Moriyoshi, Koki","first_name":"Koki"},{"full_name":"Suzuki, Misao","first_name":"Misao","last_name":"Suzuki"},{"last_name":"Kobayashi","full_name":"Kobayashi, Kazuto","first_name":"Kazuto"},{"first_name":"Toshiharu","full_name":"Nagatsu, Toshiharu","last_name":"Nagatsu"},{"full_name":"Kreitman, Robert","first_name":"Robert","last_name":"Kreitman"},{"last_name":"Pastan","full_name":"Pastan, Ira","first_name":"Ira"},{"first_name":"Shigetada","full_name":"Nakanishi, Shigetada","last_name":"Nakanishi"}],"type":"journal_article","day":"02","title":"Ablation of cerebellar Golgi cells disrupts synaptic integration involving GABA inhibition and NMDA receptor activation in motor coordination","citation":{"short":"D. Watanabe, H. Inokawa, K. Hashimoto, N. Suzuki, M. Kano, R. Shigemoto, T. Hirano, K. Toyama, S. Kaneko, M. Yokoi, K. Moriyoshi, M. Suzuki, K. Kobayashi, T. Nagatsu, R. Kreitman, I. Pastan, S. Nakanishi, Cell 95 (1998) 17–27.","ama":"Watanabe D, Inokawa H, Hashimoto K, et al. Ablation of cerebellar Golgi cells disrupts synaptic integration involving GABA inhibition and NMDA receptor activation in motor coordination. <i>Cell</i>. 1998;95(1):17-27. doi:<a href=\"https://doi.org/10.1016/S0092-8674(00)81779-1\">10.1016/S0092-8674(00)81779-1</a>","apa":"Watanabe, D., Inokawa, H., Hashimoto, K., Suzuki, N., Kano, M., Shigemoto, R., … Nakanishi, S. (1998). Ablation of cerebellar Golgi cells disrupts synaptic integration involving GABA inhibition and NMDA receptor activation in motor coordination. <i>Cell</i>. Cell Press. <a href=\"https://doi.org/10.1016/S0092-8674(00)81779-1\">https://doi.org/10.1016/S0092-8674(00)81779-1</a>","chicago":"Watanabe, Dai, Hitoshi Inokawa, Kouichi Hashimoto, Noboru Suzuki, Masanobu Kano, Ryuichi Shigemoto, Tomoo Hirano, et al. “Ablation of Cerebellar Golgi Cells Disrupts Synaptic Integration Involving GABA Inhibition and NMDA Receptor Activation in Motor Coordination.” <i>Cell</i>. Cell Press, 1998. <a href=\"https://doi.org/10.1016/S0092-8674(00)81779-1\">https://doi.org/10.1016/S0092-8674(00)81779-1</a>.","ieee":"D. Watanabe <i>et al.</i>, “Ablation of cerebellar Golgi cells disrupts synaptic integration involving GABA inhibition and NMDA receptor activation in motor coordination,” <i>Cell</i>, vol. 95, no. 1. Cell Press, pp. 17–27, 1998.","ista":"Watanabe D, Inokawa H, Hashimoto K, Suzuki N, Kano M, Shigemoto R, Hirano T, Toyama K, Kaneko S, Yokoi M, Moriyoshi K, Suzuki M, Kobayashi K, Nagatsu T, Kreitman R, Pastan I, Nakanishi S. 1998. Ablation of cerebellar Golgi cells disrupts synaptic integration involving GABA inhibition and NMDA receptor activation in motor coordination. Cell. 95(1), 17–27.","mla":"Watanabe, Dai, et al. “Ablation of Cerebellar Golgi Cells Disrupts Synaptic Integration Involving GABA Inhibition and NMDA Receptor Activation in Motor Coordination.” <i>Cell</i>, vol. 95, no. 1, Cell Press, 1998, pp. 17–27, doi:<a href=\"https://doi.org/10.1016/S0092-8674(00)81779-1\">10.1016/S0092-8674(00)81779-1</a>."},"intvolume":"        95","status":"public","publication":"Cell","quality_controlled":"1","publisher":"Cell Press","date_created":"2018-12-11T11:58:32Z","month":"10","extern":"1","page":"17 - 27"},{"pmid":1,"doi":"10.1016/s0092-8674(00)81609-8","publication_identifier":{"issn":["0092-8674"]},"date_updated":"2021-01-12T08:06:28Z","language":[{"iso":"eng"}],"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","external_id":{"pmid":["9741632"]},"title":"Natural variation in a neuropeptide Y receptor homolog modifies social behavior and food response in C. elegans","citation":{"chicago":"Bono, Mario de, and Cornelia I Bargmann. “Natural Variation in a Neuropeptide Y Receptor Homolog Modifies Social Behavior and Food Response in C. Elegans.” <i>Cell</i>. Elsevier, 1998. <a href=\"https://doi.org/10.1016/s0092-8674(00)81609-8\">https://doi.org/10.1016/s0092-8674(00)81609-8</a>.","ieee":"M. de Bono and C. I. Bargmann, “Natural variation in a neuropeptide Y receptor homolog modifies social behavior and food response in C. elegans,” <i>Cell</i>, vol. 94, no. 5. Elsevier, pp. 679–689, 1998.","ista":"de Bono M, Bargmann CI. 1998. Natural variation in a neuropeptide Y receptor homolog modifies social behavior and food response in C. elegans. Cell. 94(5), 679–689.","mla":"de Bono, Mario, and Cornelia I. Bargmann. “Natural Variation in a Neuropeptide Y Receptor Homolog Modifies Social Behavior and Food Response in C. Elegans.” <i>Cell</i>, vol. 94, no. 5, Elsevier, 1998, pp. 679–89, doi:<a href=\"https://doi.org/10.1016/s0092-8674(00)81609-8\">10.1016/s0092-8674(00)81609-8</a>.","short":"M. de Bono, C.I. Bargmann, Cell 94 (1998) 679–689.","ama":"de Bono M, Bargmann CI. Natural variation in a neuropeptide Y receptor homolog modifies social behavior and food response in C. elegans. <i>Cell</i>. 1998;94(5):679-689. doi:<a href=\"https://doi.org/10.1016/s0092-8674(00)81609-8\">10.1016/s0092-8674(00)81609-8</a>","apa":"de Bono, M., &#38; Bargmann, C. I. (1998). Natural variation in a neuropeptide Y receptor homolog modifies social behavior and food response in C. elegans. <i>Cell</i>. Elsevier. <a href=\"https://doi.org/10.1016/s0092-8674(00)81609-8\">https://doi.org/10.1016/s0092-8674(00)81609-8</a>"},"oa_version":"None","year":"1998","type":"journal_article","author":[{"id":"4E3FF80E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-8347-0443","full_name":"de Bono, Mario","first_name":"Mario","last_name":"de Bono"},{"first_name":"Cornelia I","full_name":"Bargmann, Cornelia I","last_name":"Bargmann"}],"day":"04","publication_status":"published","publisher":"Elsevier","volume":94,"status":"public","intvolume":"        94","quality_controlled":"1","publication":"Cell","issue":"5","page":"679-689","_id":"6160","date_published":"1998-09-04T00:00:00Z","abstract":[{"text":"Natural isolates of C. elegans exhibit either solitary or social feeding behavior. Solitary foragers move slowly on a bacterial lawn and disperse across it, while social foragers move rapidly on bacteria and aggregate together. A loss-of-function mutation in the npr-1 gene, which encodes a predicted G protein–coupled receptor similar to neuropeptide Y receptors, causes a solitary strain to take on social behavior. Two isoforms of NPR-1 that differ at a single residue occur in the wild. One isoform, NPR-1 215F, is found exclusively in social strains, while the other isoform, NPR-1 215V, is found exclusively in solitary strains. An NPR-1 215V transgene can induce solitary feeding behavior in a wild social strain. Thus, isoforms of a putative neuropeptide receptor generate natural variation in C. elegans feeding behavior.","lang":"eng"}],"date_created":"2019-03-21T10:32:06Z","extern":"1","month":"09"},{"article_processing_charge":"No","issue":"5","date_published":"1995-02-10T00:00:00Z","_id":"2559","abstract":[{"lang":"eng","text":"Taking advantage of the restricted expression of metabotropic glutamate receptor subtype 6 (mGIuR6) in retinal ON bipolar cells, we generated knockout mice lacking mGIuR6 expression. The homozygous mutant mice showed a loss of ON responses but unchanged OFF responses to light. The mutant mice displayed no obvious changes in retinal cell organization nor in the projection of optic fibers to the brain. Furthermore, the mGIuR6-deficient mice showed visual behavioral responses to light stimulation as examined by shuttle box avoidance behavior experiments using light exposure as a conditioned stimulus. The results demonstrate that mGIuR6 is essential in synaptic transmission to the ON bipolar cell and that the OFF response provides an important means for transmitting visual information."}],"publication_status":"published","main_file_link":[{"open_access":"1","url":"https://www.sciencedirect.com/science/article/pii/0092867495903542"}],"oa":1,"volume":80,"article_type":"original","publist_id":"4339","year":"1995","oa_version":"Published Version","external_id":{"pmid":["7889569"]},"date_updated":"2022-06-28T13:27:50Z","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","publication_identifier":{"issn":["0092-8674"]},"page":"757 - 765","month":"02","extern":"1","date_created":"2018-12-11T11:58:23Z","publisher":"Cell Press","publication":"Cell","quality_controlled":"1","status":"public","intvolume":"        80","citation":{"ama":"Masu M, Iwakabe H, Tagawa Y, et al. Specific deficit of the ON response in visual transmission by targeted disruption of the mGIuR6 gene. <i>Cell</i>. 1995;80(5):757-765. doi:<a href=\"https://doi.org/10.1016/0092-8674(95)90354-2\">10.1016/0092-8674(95)90354-2</a>","apa":"Masu, M., Iwakabe, H., Tagawa, Y., Miyoshi, T., Yamashita, M., Fukuda, Y., … Nakanishi, S. (1995). Specific deficit of the ON response in visual transmission by targeted disruption of the mGIuR6 gene. <i>Cell</i>. Cell Press. <a href=\"https://doi.org/10.1016/0092-8674(95)90354-2\">https://doi.org/10.1016/0092-8674(95)90354-2</a>","short":"M. Masu, H. Iwakabe, Y. Tagawa, T. Miyoshi, M. Yamashita, Y. Fukuda, H. Sasaki, K. Hiroi, Y. Nakamura, R. Shigemoto, M. Takada, K. Nakamura, K. Nakao, M. Katsuki, S. Nakanishi, Cell 80 (1995) 757–765.","mla":"Masu, Masayuki, et al. “Specific Deficit of the ON Response in Visual Transmission by Targeted Disruption of the MGIuR6 Gene.” <i>Cell</i>, vol. 80, no. 5, Cell Press, 1995, pp. 757–65, doi:<a href=\"https://doi.org/10.1016/0092-8674(95)90354-2\">10.1016/0092-8674(95)90354-2</a>.","chicago":"Masu, Masayuki, Hideki Iwakabe, Yoshiaki Tagawa, Tomomitsu Miyoshi, Masayuki Yamashita, Yutaka Fukuda, Hitoshi Sasaki, et al. “Specific Deficit of the ON Response in Visual Transmission by Targeted Disruption of the MGIuR6 Gene.” <i>Cell</i>. Cell Press, 1995. <a href=\"https://doi.org/10.1016/0092-8674(95)90354-2\">https://doi.org/10.1016/0092-8674(95)90354-2</a>.","ista":"Masu M, Iwakabe H, Tagawa Y, Miyoshi T, Yamashita M, Fukuda Y, Sasaki H, Hiroi K, Nakamura Y, Shigemoto R, Takada M, Nakamura K, Nakao K, Katsuki M, Nakanishi S. 1995. Specific deficit of the ON response in visual transmission by targeted disruption of the mGIuR6 gene. Cell. 80(5), 757–765.","ieee":"M. Masu <i>et al.</i>, “Specific deficit of the ON response in visual transmission by targeted disruption of the mGIuR6 gene,” <i>Cell</i>, vol. 80, no. 5. Cell Press, pp. 757–765, 1995."},"title":"Specific deficit of the ON response in visual transmission by targeted disruption of the mGIuR6 gene","day":"10","type":"journal_article","author":[{"first_name":"Masayuki","full_name":"Masu, Masayuki","last_name":"Masu"},{"last_name":"Iwakabe","full_name":"Iwakabe, Hideki","first_name":"Hideki"},{"last_name":"Tagawa","full_name":"Tagawa, Yoshiaki","first_name":"Yoshiaki"},{"full_name":"Miyoshi, Tomomitsu","first_name":"Tomomitsu","last_name":"Miyoshi"},{"first_name":"Masayuki","full_name":"Yamashita, Masayuki","last_name":"Yamashita"},{"last_name":"Fukuda","first_name":"Yutaka","full_name":"Fukuda, Yutaka"},{"last_name":"Sasaki","first_name":"Hitoshi","full_name":"Sasaki, Hitoshi"},{"last_name":"Hiroi","first_name":"Kano","full_name":"Hiroi, Kano"},{"last_name":"Nakamura","full_name":"Nakamura, Yasuhisa","first_name":"Yasuhisa"},{"orcid":"0000-0001-8761-9444","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","first_name":"Ryuichi","full_name":"Shigemoto, Ryuichi","last_name":"Shigemoto"},{"last_name":"Takada","full_name":"Takada, Masahiko","first_name":"Masahiko"},{"last_name":"Nakamura","full_name":"Nakamura, Kenji","first_name":"Kenji"},{"last_name":"Nakao","first_name":"Kazuki","full_name":"Nakao, Kazuki"},{"full_name":"Katsuki, Motoya","first_name":"Motoya","last_name":"Katsuki"},{"last_name":"Nakanishi","full_name":"Nakanishi, Shigetada","first_name":"Shigetada"}],"pmid":1,"acknowledgement":"We thank Drs. N. Mizuno, M. Iso, M. Tachibana, A. Kaneko, M. Tessier-Lavigne, and T. Hensch for useful advice and A. Uesugi for photographic assistance. This work is supported by grants in aid for specially promoted research, for scientific research on priority areas, and for scientific research (A) from the Ministry of Education, Science, and Culture in Japan and by grants from the Ministry of Health and Welfare of Japan, the Sankyo Foundation, and the Senri Life Science Foundation.","language":[{"iso":"eng"}],"doi":"10.1016/0092-8674(95)90354-2"},{"publisher":"Cell Press","intvolume":"        77","status":"public","publication":"Cell","quality_controlled":"1","page":"361 - 369","date_created":"2018-12-11T11:58:21Z","month":"05","extern":"1","pmid":1,"acknowledgement":"We thank M. Tachibana for technical advice concerning dissociated bipolar cell preparation, Y. Honda for advice \r\nconcerning RCS rat experiments, and A. Uesugi for photographic assistance. This work is partly supported by research grants from the Ministry of Education, Science, and Culture of Japan and from the Ministry of Health and Welfare of\r\nJapan. ","doi":"10.1016/0092-8674(94)90151-1","language":[{"iso":"eng"}],"title":"Developmentally regulated postsynaptic localization of a metabotropic glutamate receptor in rat rod bipolar cells","citation":{"mla":"Nomura, Akinori, et al. “Developmentally Regulated Postsynaptic Localization of a Metabotropic Glutamate Receptor in Rat Rod Bipolar Cells.” <i>Cell</i>, vol. 77, no. 3, Cell Press, 1994, pp. 361–69, doi:<a href=\"https://doi.org/10.1016/0092-8674(94)90151-1\">10.1016/0092-8674(94)90151-1</a>.","ista":"Nomura A, Shigemoto R, Nakamura Y, Okamoto N, Mizuno N, Nakanishi S. 1994. Developmentally regulated postsynaptic localization of a metabotropic glutamate receptor in rat rod bipolar cells. Cell. 77(3), 361–369.","ieee":"A. Nomura, R. Shigemoto, Y. Nakamura, N. Okamoto, N. Mizuno, and S. Nakanishi, “Developmentally regulated postsynaptic localization of a metabotropic glutamate receptor in rat rod bipolar cells,” <i>Cell</i>, vol. 77, no. 3. Cell Press, pp. 361–369, 1994.","chicago":"Nomura, Akinori, Ryuichi Shigemoto, Yasuhisa Nakamura, Naoyuki Okamoto, Noboru Mizuno, and Shigetada Nakanishi. “Developmentally Regulated Postsynaptic Localization of a Metabotropic Glutamate Receptor in Rat Rod Bipolar Cells.” <i>Cell</i>. Cell Press, 1994. <a href=\"https://doi.org/10.1016/0092-8674(94)90151-1\">https://doi.org/10.1016/0092-8674(94)90151-1</a>.","apa":"Nomura, A., Shigemoto, R., Nakamura, Y., Okamoto, N., Mizuno, N., &#38; Nakanishi, S. (1994). Developmentally regulated postsynaptic localization of a metabotropic glutamate receptor in rat rod bipolar cells. <i>Cell</i>. Cell Press. <a href=\"https://doi.org/10.1016/0092-8674(94)90151-1\">https://doi.org/10.1016/0092-8674(94)90151-1</a>","ama":"Nomura A, Shigemoto R, Nakamura Y, Okamoto N, Mizuno N, Nakanishi S. Developmentally regulated postsynaptic localization of a metabotropic glutamate receptor in rat rod bipolar cells. <i>Cell</i>. 1994;77(3):361-369. doi:<a href=\"https://doi.org/10.1016/0092-8674(94)90151-1\">10.1016/0092-8674(94)90151-1</a>","short":"A. Nomura, R. Shigemoto, Y. Nakamura, N. Okamoto, N. Mizuno, S. Nakanishi, Cell 77 (1994) 361–369."},"author":[{"first_name":"Akinori","full_name":"Nomura, Akinori","last_name":"Nomura"},{"last_name":"Shigemoto","full_name":"Shigemoto, Ryuichi","first_name":"Ryuichi","orcid":"0000-0001-8761-9444","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Yasuhisa","full_name":"Nakamura, Yasuhisa","last_name":"Nakamura"},{"last_name":"Okamoto","first_name":"Naoyuki","full_name":"Okamoto, Naoyuki"},{"first_name":"Noboru","full_name":"Mizuno, Noboru","last_name":"Mizuno"},{"last_name":"Nakanishi","first_name":"Shigetada","full_name":"Nakanishi, Shigetada"}],"type":"journal_article","day":"06","main_file_link":[{"url":"https://www.sciencedirect.com/science/article/pii/0092867494901511?via%3Dihub"}],"publication_status":"published","volume":77,"article_processing_charge":"No","issue":"3","_id":"2554","date_published":"1994-05-06T00:00:00Z","abstract":[{"lang":"eng","text":"The retinal bipolar cell receiving glutamate transmission from photoreceptors mediates a key process in segregating visual signals into ON center and OFF center pathways. This transmission involves a G protein- coupled metabotropic glutamate receptor (mGluR). Immunocytochemical and immunoelectron microscopic studies indicate the restricted localization of a specific mGluR subtype, mGluR6, at the postsynaptic site of the rat rod bipolar cell. This specialization is developmentally regulated: mGluR6 is initially distributed in both the soma and dendrites and is finally concentrated on the postsynaptic site. The mGluR6 localization is reversed when photoreceptors degenerate in the mutant rat with retinal dystrophy. Evidence is thus presented indicating specialized, developmentally regulated receptor distribution in the central nervous system and the crucial role of mGluR6 in photoreceptor-bipolar cell synaptic transmission."}],"publication_identifier":{"issn":["0092-8674"]},"external_id":{"pmid":["8181056"]},"scopus_import":"1","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","date_updated":"2022-06-07T14:28:33Z","oa_version":"None","year":"1994","article_type":"original","publist_id":"4344"}]