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Shootin1: a protein involved in the organization of an asymmetric signal for neuronal polarization
Neurons have the remarkable ability to polarize even in symmetrical in vitro environments. Although recent studies have shown that asymmetric intracellular signals can induce neuronal polarization, it remains unclear how these polarized signals are organized without asymmetric cues. We describe a no...
Autores principales: | , , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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The Rockefeller University Press
2006
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2064506/ https://www.ncbi.nlm.nih.gov/pubmed/17030985 http://dx.doi.org/10.1083/jcb.200604160 |
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author | Toriyama, Michinori Shimada, Tadayuki Kim, Ki Bum Mitsuba, Mari Nomura, Eiko Katsuta, Kazuhiro Sakumura, Yuichi Roepstorff, Peter Inagaki, Naoyuki |
author_facet | Toriyama, Michinori Shimada, Tadayuki Kim, Ki Bum Mitsuba, Mari Nomura, Eiko Katsuta, Kazuhiro Sakumura, Yuichi Roepstorff, Peter Inagaki, Naoyuki |
author_sort | Toriyama, Michinori |
collection | PubMed |
description | Neurons have the remarkable ability to polarize even in symmetrical in vitro environments. Although recent studies have shown that asymmetric intracellular signals can induce neuronal polarization, it remains unclear how these polarized signals are organized without asymmetric cues. We describe a novel protein, named shootin1, that became up-regulated during polarization of hippocampal neurons and began fluctuating accumulation among multiple neurites. Eventually, shootin1 accumulated asymmetrically in a single neurite, which led to axon induction for polarization. Disturbing the asymmetric organization of shootin1 by excess shootin1 disrupted polarization, whereas repressing shootin1 expression inhibited polarization. Overexpression and RNA interference data suggest that shootin1 is required for spatially localized phosphoinositide-3-kinase activity. Shootin1 was transported anterogradely to the growth cones and diffused back to the soma; inhibiting this transport prevented its asymmetric accumulation in neurons. We propose that shootin1 is involved in the generation of internal asymmetric signals required for neuronal polarization. |
format | Text |
id | pubmed-2064506 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2006 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-20645062007-11-29 Shootin1: a protein involved in the organization of an asymmetric signal for neuronal polarization Toriyama, Michinori Shimada, Tadayuki Kim, Ki Bum Mitsuba, Mari Nomura, Eiko Katsuta, Kazuhiro Sakumura, Yuichi Roepstorff, Peter Inagaki, Naoyuki J Cell Biol Research Articles Neurons have the remarkable ability to polarize even in symmetrical in vitro environments. Although recent studies have shown that asymmetric intracellular signals can induce neuronal polarization, it remains unclear how these polarized signals are organized without asymmetric cues. We describe a novel protein, named shootin1, that became up-regulated during polarization of hippocampal neurons and began fluctuating accumulation among multiple neurites. Eventually, shootin1 accumulated asymmetrically in a single neurite, which led to axon induction for polarization. Disturbing the asymmetric organization of shootin1 by excess shootin1 disrupted polarization, whereas repressing shootin1 expression inhibited polarization. Overexpression and RNA interference data suggest that shootin1 is required for spatially localized phosphoinositide-3-kinase activity. Shootin1 was transported anterogradely to the growth cones and diffused back to the soma; inhibiting this transport prevented its asymmetric accumulation in neurons. We propose that shootin1 is involved in the generation of internal asymmetric signals required for neuronal polarization. The Rockefeller University Press 2006-10-09 /pmc/articles/PMC2064506/ /pubmed/17030985 http://dx.doi.org/10.1083/jcb.200604160 Text en Copyright © 2006, The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Research Articles Toriyama, Michinori Shimada, Tadayuki Kim, Ki Bum Mitsuba, Mari Nomura, Eiko Katsuta, Kazuhiro Sakumura, Yuichi Roepstorff, Peter Inagaki, Naoyuki Shootin1: a protein involved in the organization of an asymmetric signal for neuronal polarization |
title | Shootin1: a protein involved in the organization of an asymmetric signal for neuronal polarization |
title_full | Shootin1: a protein involved in the organization of an asymmetric signal for neuronal polarization |
title_fullStr | Shootin1: a protein involved in the organization of an asymmetric signal for neuronal polarization |
title_full_unstemmed | Shootin1: a protein involved in the organization of an asymmetric signal for neuronal polarization |
title_short | Shootin1: a protein involved in the organization of an asymmetric signal for neuronal polarization |
title_sort | shootin1: a protein involved in the organization of an asymmetric signal for neuronal polarization |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2064506/ https://www.ncbi.nlm.nih.gov/pubmed/17030985 http://dx.doi.org/10.1083/jcb.200604160 |
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