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本文引用的文献

1
Axons and dendrites originate from neuroepithelial-like processes of retinal bipolar cells.轴突和树突起源于视网膜双极细胞的神经上皮样突起。
Nat Neurosci. 2006 Jan;9(1):85-92. doi: 10.1038/nn1615. Epub 2005 Dec 11.
2
Mutation of the calcium channel gene Cacna1f disrupts calcium signaling, synaptic transmission and cellular organization in mouse retina.钙通道基因Cacna1f的突变会破坏小鼠视网膜中的钙信号传导、突触传递和细胞组织。
Hum Mol Genet. 2005 Oct 15;14(20):3035-46. doi: 10.1093/hmg/ddi336. Epub 2005 Sep 9.
3
Rhodopsin-iCre transgenic mouse line for Cre-mediated rod-specific gene targeting.用于 Cre 介导的视杆细胞特异性基因靶向的视紫红质-iCre 转基因小鼠品系。
Genesis. 2005 Feb;41(2):73-80. doi: 10.1002/gene.20097.
4
A retinal neuronal developmental wave of retinoschisin expression begins in ganglion cells during layer formation.视网膜分裂蛋白表达的视网膜神经元发育波在神经节细胞层形成过程中开始。
Invest Ophthalmol Vis Sci. 2004 Sep;45(9):3302-12. doi: 10.1167/iovs.04-0156.
5
A retinal-specific regulator of G-protein signaling interacts with Galpha(o) and accelerates an expressed metabotropic glutamate receptor 6 cascade.一种视网膜特异性G蛋白信号调节剂与Gα(o)相互作用,并加速表达的代谢型谷氨酸受体6信号级联反应。
J Neurosci. 2004 Jun 23;24(25):5684-93. doi: 10.1523/JNEUROSCI.0492-04.2004.
6
Selective transmission of single photon responses by saturation at the rod-to-rod bipolar synapse.在视杆细胞到双极细胞突触处通过饱和实现单光子反应的选择性传递。
Neuron. 2004 Feb 5;41(3):431-43. doi: 10.1016/s0896-6273(04)00005-4.
7
Absence of the RGS9.Gbeta5 GTPase-activating complex in photoreceptors of the R9AP knockout mouse.R9AP基因敲除小鼠光感受器中RGS9.Gbeta5 GTP酶激活复合物缺失。
J Biol Chem. 2004 Jan 16;279(3):1581-4. doi: 10.1074/jbc.C300456200. Epub 2003 Nov 18.
8
The DEP domain determines subcellular targeting of the GTPase activating protein RGS9 in vivo.DEP结构域在体内决定了GTP酶激活蛋白RGS9的亚细胞定位。
J Neurosci. 2003 Nov 12;23(32):10175-81. doi: 10.1523/JNEUROSCI.23-32-10175.2003.
9
Immunohistochemical analysis of the outer plexiform layer in the nob mouse shows no abnormalities.对nob小鼠外网状层的免疫组织化学分析显示无异常。
Vis Neurosci. 2003 May-Jun;20(3):267-72. doi: 10.1017/s0952523803203059.
10
Prolonged photoresponses and defective adaptation in rods of Gbeta5-/- mice.Gβ5基因敲除小鼠视杆细胞中的光反应延长及适应性缺陷
J Neurosci. 2003 Aug 6;23(18):6965-71. doi: 10.1523/JNEUROSCI.23-18-06965.2003.

视网膜ON双极细胞的正常光反应和形态需要Gbeta5。

Gbeta5 is required for normal light responses and morphology of retinal ON-bipolar cells.

作者信息

Rao Anjali, Dallman Rebecca, Henderson Scott, Chen Ching-Kang

机构信息

Department of Biochemistry and Molecular Biology, Virginia Commonwealth University, Richmond, Virginia 23298, USA.

出版信息

J Neurosci. 2007 Dec 19;27(51):14199-204. doi: 10.1523/JNEUROSCI.4934-07.2007.

DOI:10.1523/JNEUROSCI.4934-07.2007
PMID:18094259
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6673526/
Abstract

Gbeta5 exists as two splice variants, Gbeta5-S and Gbeta5-L, which interact with and stabilize the R7 members of the regulators of G-protein signaling (RGSs): RGS6, RGS7, RGS9, and RGS11. Although the role of Gbeta5-L and RGS9-1 is established in photoreceptors, the physiological functions of Gbeta5-S and other R7 RGS proteins remain unclear. We found that the electroretinogram of Gbeta5-/- mice lacks the b-wave component and that Gbeta5-S and RGS11 colocalize with Go alpha at the tips of the ON-bipolar cell dendrites. Unexpectedly, we found a significant reduction in the number of synaptic triads in the outer plexiform layer (OPL) of the Gbeta5-/- mice, which is evident at postnatal day 14. Transgenic expression of Gbeta5-L in rods failed to rescue the b-wave or the OPL defects. These results indicate that Gbeta5-S is indispensable for OPL integrity and normal light responses of the retina.

摘要

Gβ5 以两种剪接变体 Gβ5-S 和 Gβ5-L 的形式存在,它们与 G 蛋白信号调节因子(RGSs)的 R7 成员相互作用并使其稳定,这些成员包括 RGS6、RGS7、RGS9 和 RGS11。尽管 Gβ5-L 和 RGS9-1 在光感受器中的作用已得到证实,但 Gβ5-S 和其他 R7 RGS 蛋白的生理功能仍不清楚。我们发现 Gβ5-/- 小鼠的视网膜电图缺乏 b 波成分,并且 Gβ5-S 和 RGS11 在 ON 双极细胞树突末端与 Goα 共定位。出乎意料的是,我们发现 Gβ5-/- 小鼠外网状层(OPL)中突触三联体的数量显著减少,这在出生后第 14 天很明显。在视杆细胞中转基因表达 Gβ5-L 未能挽救 b 波或 OPL 缺陷。这些结果表明,Gβ5-S 对于视网膜的 OPL 完整性和正常光反应是不可或缺的。