A conserved Cys-loop receptor aspartate residue in the M3-M4 cytoplasmic loop is required for GABAA receptor assembly.
about
Differential protein structural disturbances and suppression of assembly partners produced by nonsense GABRG2 epilepsy mutations: implications for disease phenotypic heterogeneity.Homeostatic strengthening of inhibitory synapses is mediated by the accumulation of GABA(A) receptors.Length and amino acid sequence of peptides substituted for the 5-HT3A receptor M3M4 loop may affect channel expression and desensitizationCo-expression of γ2 subunits hinders processing of N-linked glycans attached to the N104 glycosylation sites of GABAA receptor β2 subunits.GABA(A) receptor alpha1 subunit mutation A322D associated with autosomal dominant juvenile myoclonic epilepsy reduces the expression and alters the composition of wild type GABA(A) receptorsRIC-3 exclusively enhances the surface expression of human homomeric 5-hydroxytryptamine type 3A (5-HT3A) receptors despite direct interactions with 5-HT3A, -C, -D, and -E subunitsGlycosylation of {beta}2 subunits regulates GABAA receptor biogenesis and channel gatingThe effect of HSP-causing mutations in SPG3A and NIPA1 on the assembly, trafficking, and interaction between atlastin-1 and NIPA1A de novo missense mutation of GABRB2 causes early myoclonic encephalopathyDiscrete M3-M4 intracellular loop subdomains control specific aspects of γ-aminobutyric acid type A receptor function.The minimum M3-M4 loop length of neurotransmitter-activated pentameric receptors is critical for the structural integrity of cytoplasmic portals.Impaired surface αβγ GABA(A) receptor expression in familial epilepsy due to a GABRG2 frameshift mutationAltered cortical GABAA receptor composition, physiology, and endocytosis in a mouse model of a human genetic absence epilepsy syndrome.Alternatively spliced isoforms of TRIP8b differentially control h channel trafficking and function.An intracellular redox sensor for reactive oxygen species at the M3-M4 linker of GABAA ρ1 receptors.Assembly of nicotinic and other Cys-loop receptors.The GABRG2 nonsense mutation, Q40X, associated with Dravet syndrome activated NMD and generated a truncated subunit that was partially rescued by aminoglycoside-induced stop codon read-through.Slow degradation and aggregation in vitro of mutant GABAA receptor gamma2(Q351X) subunits associated with epilepsyThree epilepsy-associated GABRG2 missense mutations at the γ+/β- interface disrupt GABAA receptor assembly and trafficking by similar mechanisms but to different extents.Negative modulation of the GABAA ρ1 receptor function by l-cysteine.
P2860
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P2860
A conserved Cys-loop receptor aspartate residue in the M3-M4 cytoplasmic loop is required for GABAA receptor assembly.
description
2008 nî lūn-bûn
@nan
2008年の論文
@ja
2008年学术文章
@wuu
2008年学术文章
@zh
2008年学术文章
@zh-cn
2008年学术文章
@zh-hans
2008年学术文章
@zh-my
2008年学术文章
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2008年學術文章
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2008年學術文章
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name
A conserved Cys-loop receptor ...... d for GABAA receptor assembly.
@en
A conserved Cys-loop receptor ...... d for GABAA receptor assembly.
@nl
type
label
A conserved Cys-loop receptor ...... d for GABAA receptor assembly.
@en
A conserved Cys-loop receptor ...... d for GABAA receptor assembly.
@nl
prefLabel
A conserved Cys-loop receptor ...... d for GABAA receptor assembly.
@en
A conserved Cys-loop receptor ...... d for GABAA receptor assembly.
@nl
P2093
P2860
P356
P1476
A conserved Cys-loop receptor ...... d for GABAA receptor assembly.
@en
P2093
Emmanuel J Botzolakis
Robert L Macdonald
P2860
P304
29740-29752
P356
10.1074/JBC.M802856200
P407
P577
2008-08-21T00:00:00Z