---
_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.
article_processing_charge: No
article_type: original
author:
- first_name: Tobias C.
full_name: Walther, Tobias C.
last_name: Walther
- first_name: Annabelle
full_name: Alves, Annabelle
last_name: Alves
- first_name: Helen
full_name: Pickersgill, Helen
last_name: Pickersgill
- first_name: Isabelle
full_name: Loı̈odice, Isabelle
last_name: Loı̈odice
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
- first_name: Vincent
full_name: Galy, Vincent
last_name: Galy
- first_name: Bastian B.
full_name: Hülsmann, Bastian B.
last_name: Hülsmann
- first_name: Thomas
full_name: Köcher, Thomas
last_name: Köcher
- first_name: Matthias
full_name: Wilm, Matthias
last_name: Wilm
- first_name: Terry
full_name: Allen, Terry
last_name: Allen
- first_name: Iain W.
full_name: Mattaj, Iain W.
last_name: Mattaj
- first_name: Valérie
full_name: Doye, Valérie
last_name: Doye
citation:
ama: Walther TC, Alves A, Pickersgill H, et al. The conserved Nup107-160 complex
is critical for nuclear pore complex assembly. Cell. 2003;113(2):195-206.
doi:10.1016/s0092-8674(03)00235-6
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. Cell. Elsevier. https://doi.org/10.1016/s0092-8674(03)00235-6
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.” Cell. Elsevier,
2003. https://doi.org/10.1016/s0092-8674(03)00235-6.
ieee: T. C. Walther et al., “The conserved Nup107-160 complex is critical
for nuclear pore complex assembly,” Cell, vol. 113, no. 2. Elsevier, pp.
195–206, 2003.
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.
mla: Walther, Tobias C., et al. “The Conserved Nup107-160 Complex Is Critical for
Nuclear Pore Complex Assembly.” Cell, vol. 113, no. 2, Elsevier, 2003,
pp. 195–206, doi:10.1016/s0092-8674(03)00235-6.
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.
date_created: 2022-04-07T07:57:10Z
date_published: 2003-04-17T00:00:00Z
date_updated: 2022-07-18T08:57:42Z
day: '17'
doi: 10.1016/s0092-8674(03)00235-6
extern: '1'
external_id:
pmid:
- '12705868'
intvolume: ' 113'
issue: '2'
keyword:
- General Biochemistry
- Genetics and Molecular Biology
language:
- iso: eng
month: '04'
oa_version: Published Version
page: 195-206
pmid: 1
publication: Cell
publication_identifier:
issn:
- 0092-8674
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: The conserved Nup107-160 complex is critical for nuclear pore complex assembly
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 113
year: '2003'
...
---
_id: '2989'
abstract:
- lang: eng
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.
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.
article_processing_charge: No
article_type: original
author:
- first_name: Jirí
full_name: Friml, Jirí
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
- first_name: Eva
full_name: Benková, Eva
id: 38F4F166-F248-11E8-B48F-1D18A9856A87
last_name: Benková
orcid: 0000-0002-8510-9739
- first_name: Ikram
full_name: Blilou, Ikram
last_name: Blilou
- first_name: Justyna
full_name: Wiśniewska, Justyna
last_name: Wiśniewska
- first_name: Thorsten
full_name: Hamann, Thorsten
last_name: Hamann
- first_name: Karin
full_name: Ljung, Karin
last_name: Ljung
- first_name: Scott
full_name: Woody, Scott
last_name: Woody
- first_name: Göran
full_name: Sandberg, Göran
last_name: Sandberg
- first_name: Ben
full_name: Scheres, Ben
last_name: Scheres
- first_name: Gerd
full_name: Jürgens, Gerd
last_name: Jürgens
- first_name: Klaus
full_name: Palme, Klaus
last_name: Palme
citation:
ama: Friml J, Benková E, Blilou I, et al. AtPIN4 mediates sink-driven auxin gradients
and root patterning in Arabidopsis. Cell. 2002;108(5):661-673. doi:10.1016/S0092-8674(02)00656-6
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. Cell. Cell Press. https://doi.org/10.1016/S0092-8674(02)00656-6
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.” Cell. Cell Press, 2002. https://doi.org/10.1016/S0092-8674(02)00656-6.
ieee: J. Friml et al., “AtPIN4 mediates sink-driven auxin gradients and root
patterning in Arabidopsis,” Cell, vol. 108, no. 5. Cell Press, pp. 661–673,
2002.
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.
mla: Friml, Jiří, et al. “AtPIN4 Mediates Sink-Driven Auxin Gradients and Root Patterning
in Arabidopsis.” Cell, vol. 108, no. 5, Cell Press, 2002, pp. 661–73, doi:10.1016/S0092-8674(02)00656-6.
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.
date_created: 2018-12-11T12:00:43Z
date_published: 2002-03-08T00:00:00Z
date_updated: 2023-07-17T11:57:40Z
day: '08'
doi: 10.1016/S0092-8674(02)00656-6
extern: '1'
external_id:
pmid:
- '11893337'
intvolume: ' 108'
issue: '5'
language:
- iso: eng
month: '03'
oa_version: None
page: 661 - 673
pmid: 1
publication: Cell
publication_identifier:
issn:
- 0092-8674
publication_status: published
publisher: Cell Press
publist_id: '3713'
quality_controlled: '1'
scopus_import: '1'
status: public
title: AtPIN4 mediates sink-driven auxin gradients and root patterning in Arabidopsis
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 108
year: '2002'
...
---
_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.
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"
article_processing_charge: No
article_type: original
author:
- first_name: Dai
full_name: Watanabe, Dai
last_name: Watanabe
- first_name: Hitoshi
full_name: Inokawa, Hitoshi
last_name: Inokawa
- first_name: Kouichi
full_name: Hashimoto, Kouichi
last_name: Hashimoto
- first_name: Noboru
full_name: Suzuki, Noboru
last_name: Suzuki
- first_name: Masanobu
full_name: Kano, Masanobu
last_name: Kano
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Tomoo
full_name: Hirano, Tomoo
last_name: Hirano
- first_name: Keisuke
full_name: Toyama, Keisuke
last_name: Toyama
- first_name: Satoshi
full_name: Kaneko, Satoshi
last_name: Kaneko
- first_name: Mineto
full_name: Yokoi, Mineto
last_name: Yokoi
- first_name: Koki
full_name: Moriyoshi, Koki
last_name: Moriyoshi
- first_name: Misao
full_name: Suzuki, Misao
last_name: Suzuki
- first_name: Kazuto
full_name: Kobayashi, Kazuto
last_name: Kobayashi
- first_name: Toshiharu
full_name: Nagatsu, Toshiharu
last_name: Nagatsu
- first_name: Robert
full_name: Kreitman, Robert
last_name: Kreitman
- first_name: Ira
full_name: Pastan, Ira
last_name: Pastan
- first_name: Shigetada
full_name: Nakanishi, Shigetada
last_name: Nakanishi
citation:
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. Cell. 1998;95(1):17-27. doi:10.1016/S0092-8674(00)81779-1
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.
Cell. Cell Press. https://doi.org/10.1016/S0092-8674(00)81779-1
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.” Cell. Cell Press, 1998. https://doi.org/10.1016/S0092-8674(00)81779-1.
ieee: D. Watanabe et al., “Ablation of cerebellar Golgi cells disrupts synaptic
integration involving GABA inhibition and NMDA receptor activation in motor coordination,”
Cell, 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.”
Cell, vol. 95, no. 1, Cell Press, 1998, pp. 17–27, doi:10.1016/S0092-8674(00)81779-1.
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.
date_created: 2018-12-11T11:58:32Z
date_published: 1998-10-02T00:00:00Z
date_updated: 2022-08-31T13:46:20Z
day: '02'
doi: 10.1016/S0092-8674(00)81779-1
extern: '1'
external_id:
pmid:
- '9778244 '
intvolume: ' 95'
issue: '1'
language:
- iso: eng
month: '10'
oa_version: None
page: 17 - 27
pmid: 1
publication: Cell
publication_identifier:
issn:
- 0092-8674
publication_status: published
publisher: Cell Press
publist_id: '4312'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Ablation of cerebellar Golgi cells disrupts synaptic integration involving
GABA inhibition and NMDA receptor activation in motor coordination
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 95
year: '1998'
...
---
_id: '6160'
abstract:
- lang: eng
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.
author:
- first_name: Mario
full_name: de Bono, Mario
id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
last_name: de Bono
orcid: 0000-0001-8347-0443
- first_name: Cornelia I
full_name: Bargmann, Cornelia I
last_name: Bargmann
citation:
ama: de Bono M, Bargmann CI. Natural variation in a neuropeptide Y receptor homolog
modifies social behavior and food response in C. elegans. Cell. 1998;94(5):679-689.
doi:10.1016/s0092-8674(00)81609-8
apa: de Bono, M., & Bargmann, C. I. (1998). Natural variation in a neuropeptide
Y receptor homolog modifies social behavior and food response in C. elegans. Cell.
Elsevier. https://doi.org/10.1016/s0092-8674(00)81609-8
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.”
Cell. Elsevier, 1998. https://doi.org/10.1016/s0092-8674(00)81609-8.
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,” Cell,
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.”
Cell, vol. 94, no. 5, Elsevier, 1998, pp. 679–89, doi:10.1016/s0092-8674(00)81609-8.
short: M. de Bono, C.I. Bargmann, Cell 94 (1998) 679–689.
date_created: 2019-03-21T10:32:06Z
date_published: 1998-09-04T00:00:00Z
date_updated: 2021-01-12T08:06:28Z
day: '04'
doi: 10.1016/s0092-8674(00)81609-8
extern: '1'
external_id:
pmid:
- '9741632'
intvolume: ' 94'
issue: '5'
language:
- iso: eng
month: '09'
oa_version: None
page: 679-689
pmid: 1
publication: Cell
publication_identifier:
issn:
- 0092-8674
publication_status: published
publisher: Elsevier
quality_controlled: '1'
status: public
title: Natural variation in a neuropeptide Y receptor homolog modifies social behavior
and food response in C. elegans
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 94
year: '1998'
...
---
_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.
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.
article_processing_charge: No
article_type: original
author:
- first_name: Masayuki
full_name: Masu, Masayuki
last_name: Masu
- first_name: Hideki
full_name: Iwakabe, Hideki
last_name: Iwakabe
- first_name: Yoshiaki
full_name: Tagawa, Yoshiaki
last_name: Tagawa
- first_name: Tomomitsu
full_name: Miyoshi, Tomomitsu
last_name: Miyoshi
- first_name: Masayuki
full_name: Yamashita, Masayuki
last_name: Yamashita
- first_name: Yutaka
full_name: Fukuda, Yutaka
last_name: Fukuda
- first_name: Hitoshi
full_name: Sasaki, Hitoshi
last_name: Sasaki
- first_name: Kano
full_name: Hiroi, Kano
last_name: Hiroi
- first_name: Yasuhisa
full_name: Nakamura, Yasuhisa
last_name: Nakamura
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Masahiko
full_name: Takada, Masahiko
last_name: Takada
- first_name: Kenji
full_name: Nakamura, Kenji
last_name: Nakamura
- first_name: Kazuki
full_name: Nakao, Kazuki
last_name: Nakao
- first_name: Motoya
full_name: Katsuki, Motoya
last_name: Katsuki
- first_name: Shigetada
full_name: Nakanishi, Shigetada
last_name: Nakanishi
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. Cell. 1995;80(5):757-765.
doi:10.1016/0092-8674(95)90354-2
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. Cell. Cell Press. https://doi.org/10.1016/0092-8674(95)90354-2
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.” Cell.
Cell Press, 1995. https://doi.org/10.1016/0092-8674(95)90354-2.
ieee: M. Masu et al., “Specific deficit of the ON response in visual transmission
by targeted disruption of the mGIuR6 gene,” Cell, vol. 80, no. 5. Cell
Press, pp. 757–765, 1995.
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.
mla: Masu, Masayuki, et al. “Specific Deficit of the ON Response in Visual Transmission
by Targeted Disruption of the MGIuR6 Gene.” Cell, vol. 80, no. 5, Cell
Press, 1995, pp. 757–65, doi:10.1016/0092-8674(95)90354-2.
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.
date_created: 2018-12-11T11:58:23Z
date_published: 1995-02-10T00:00:00Z
date_updated: 2022-06-28T13:27:50Z
day: '10'
doi: 10.1016/0092-8674(95)90354-2
extern: '1'
external_id:
pmid:
- '7889569'
intvolume: ' 80'
issue: '5'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.sciencedirect.com/science/article/pii/0092867495903542
month: '02'
oa: 1
oa_version: Published Version
page: 757 - 765
pmid: 1
publication: Cell
publication_identifier:
issn:
- 0092-8674
publication_status: published
publisher: Cell Press
publist_id: '4339'
quality_controlled: '1'
status: public
title: Specific deficit of the ON response in visual transmission by targeted disruption
of the mGIuR6 gene
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 80
year: '1995'
...
---
_id: '2554'
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.'
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. "
article_processing_charge: No
article_type: original
author:
- first_name: Akinori
full_name: Nomura, Akinori
last_name: Nomura
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Yasuhisa
full_name: Nakamura, Yasuhisa
last_name: Nakamura
- first_name: Naoyuki
full_name: Okamoto, Naoyuki
last_name: Okamoto
- first_name: Noboru
full_name: Mizuno, Noboru
last_name: Mizuno
- first_name: Shigetada
full_name: Nakanishi, Shigetada
last_name: Nakanishi
citation:
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. Cell. 1994;77(3):361-369. doi:10.1016/0092-8674(94)90151-1
apa: 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. Cell Press. https://doi.org/10.1016/0092-8674(94)90151-1
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.” Cell.
Cell Press, 1994. https://doi.org/10.1016/0092-8674(94)90151-1.
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,” Cell, vol. 77, no. 3. Cell Press, pp.
361–369, 1994.
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.
mla: Nomura, Akinori, et al. “Developmentally Regulated Postsynaptic Localization
of a Metabotropic Glutamate Receptor in Rat Rod Bipolar Cells.” Cell, vol.
77, no. 3, Cell Press, 1994, pp. 361–69, doi:10.1016/0092-8674(94)90151-1.
short: A. Nomura, R. Shigemoto, Y. Nakamura, N. Okamoto, N. Mizuno, S. Nakanishi,
Cell 77 (1994) 361–369.
date_created: 2018-12-11T11:58:21Z
date_published: 1994-05-06T00:00:00Z
date_updated: 2022-06-07T14:28:33Z
day: '06'
doi: 10.1016/0092-8674(94)90151-1
extern: '1'
external_id:
pmid:
- '8181056'
intvolume: ' 77'
issue: '3'
language:
- iso: eng
main_file_link:
- url: https://www.sciencedirect.com/science/article/pii/0092867494901511?via%3Dihub
month: '05'
oa_version: None
page: 361 - 369
pmid: 1
publication: Cell
publication_identifier:
issn:
- 0092-8674
publication_status: published
publisher: Cell Press
publist_id: '4344'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Developmentally regulated postsynaptic localization of a metabotropic glutamate
receptor in rat rod bipolar cells
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 77
year: '1994'
...