Gbeta5 is required for normal light responses and morphology of retinal ON-bipolar cells.
about
GPR179 is required for depolarizing bipolar cell function and is mutated in autosomal-recessive complete congenital stationary night blindnessMutations in TRPM1 are a common cause of complete congenital stationary night blindnessThe R7 RGS protein family: multi-subunit regulators of neuronal G protein signalingA Naturally Occurring Canine Model of Autosomal Recessive Congenital Stationary Night BlindnessRetinal ON bipolar cells express a new PCP2 splice variant that accelerates the light responseProbing neurochemical structure and function of retinal ON bipolar cells with a transgenic mouseTargeting of RGS7/Gbeta5 to the dendritic tips of ON-bipolar cells is independent of its association with membrane anchor R7BP.Loss of the Synaptic Vesicle Protein SV2B results in reduced neurotransmission and altered synaptic vesicle protein expression in the retina.Membrane anchor R9AP potentiates GTPase-accelerating protein activity of RGS11 x Gbeta5 complex and accelerates inactivation of the mGluR6-G(o) signaling.Functional redundancy of R7 RGS proteins in ON-bipolar cell dendritesRGS7 and -11 complexes accelerate the ON-bipolar cell light response.RGS9 knockout causes a short delay in light responses of ON-bipolar cells.Plasticity of TRPM1 expression and localization in the wild type and degenerating mouse retinaSynaptic development of the mouse dorsal lateral geniculate nucleus.R9AP stabilizes RGS11-G beta5 and accelerates the early light response of ON-bipolar cellsAn allosteric regulator of R7-RGS proteins influences light-evoked activity and glutamatergic waves in the inner retina.Localization of Cacna1s to ON bipolar dendritic tips requires mGluR6-related cascade elements.A role for nyctalopin, a small leucine-rich repeat protein, in localizing the TRP melastatin 1 channel to retinal depolarizing bipolar cell dendritesKnockout of G protein β5 impairs brain development and causes multiple neurologic abnormalities in mice.Differential function of Gγ13 in rod bipolar and ON cone bipolar cells.Defective retinal depolarizing bipolar cells in regulators of G protein signaling (RGS) 7 and 11 double null mice.Regulators of G protein signaling RGS7 and RGS11 determine the onset of the light response in ON bipolar neurons.Synaptic pathology and therapeutic repair in adult retinoschisis mouse by AAV-RS1 transfer.Subcellular localization of regulator of G protein signaling RGS7 complex in neurons and transfected cells.Gβ3 is required for normal light ON responses and synaptic maintenanceModulation of mouse rod response decay by rhodopsin kinase and recoverin.LRIT3 is essential to localize TRPM1 to the dendritic tips of depolarizing bipolar cells and may play a role in cone synapse formation.Intermolecular Interaction between Anchoring Subunits Specify Subcellular Targeting and Function of RGS Proteins in Retina ON-Bipolar NeuronsAmyloid Precursor-Like Protein 2 deletion-induced retinal synaptopathy related to congenital stationary night blindness: structural, functional and molecular characteristicsLack of mGluR6-related cascade elements leads to retrograde trans-synaptic effects on rod photoreceptor synapses via matrix-associated proteins.Regulation of ON bipolar cell activity.Changes in striatal signaling induce remodeling of RGS complexes containing Gbeta5 and R7BP subunits.Comparisons of structural and functional abnormalities in mouse b-wave mutants.GNB5 Mutations Cause an Autosomal-Recessive Multisystem Syndrome with Sinus Bradycardia and Cognitive Disability.Two R7 regulator of G-protein signaling proteins shape retinal bipolar cell signaling.Retina-specific GTPase accelerator RGS11/G beta 5S/R9AP is a constitutive heterotrimer selectively targeted to mGluR6 in ON-bipolar neuronsR9AP and R7BP: traffic cops for the RGS7 family in phototransduction and neuronal GPCR signaling.Structure, function, and localization of Gβ5-RGS complexes.LRIT3 Differentially Affects Connectivity and Synaptic Transmission of Cones to ON- and OFF-Bipolar Cells.GPR179 is required for high sensitivity of the mGluR6 signaling cascade in depolarizing bipolar cells.
P2860
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P2860
Gbeta5 is required for normal light responses and morphology of retinal ON-bipolar cells.
description
2007 nî lūn-bûn
@nan
2007年の論文
@ja
2007年学术文章
@wuu
2007年学术文章
@zh-cn
2007年学术文章
@zh-hans
2007年学术文章
@zh-my
2007年学术文章
@zh-sg
2007年學術文章
@yue
2007年學術文章
@zh
2007年學術文章
@zh-hant
name
Gbeta5 is required for normal light responses and morphology of retinal ON-bipolar cells.
@en
Gbeta5 is required for normal light responses and morphology of retinal ON-bipolar cells.
@nl
type
label
Gbeta5 is required for normal light responses and morphology of retinal ON-bipolar cells.
@en
Gbeta5 is required for normal light responses and morphology of retinal ON-bipolar cells.
@nl
prefLabel
Gbeta5 is required for normal light responses and morphology of retinal ON-bipolar cells.
@en
Gbeta5 is required for normal light responses and morphology of retinal ON-bipolar cells.
@nl
P2093
P1476
Gbeta5 is required for normal light responses and morphology of retinal ON-bipolar cells
@en
P2093
Anjali Rao
Ching-Kang Chen
Rebecca Dallman
P304
14199-14204
P356
10.1523/JNEUROSCI.4934-07.2007
P407
P577
2007-12-01T00:00:00Z