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individuals with loss-of-function GNB5 alleles had more severe symptoms, including substantial developmental delay, speech defects, severe hypotonia, pathological gastro-esophageal reflux, retinal disease, and sinus-node dysfunction, whereas related heterozygotes harboring missense variants presented with a clinically milder phenotype
Results suggest that D2R can interact with and stabilize the Gb5 protein, independently of R7 G protein signaling (RGS) proteins.
The intrinsic resistance to TRAIL-triggered apoptosis of colon cancer cells is overcome by antagonization of Gbeta5.
Type 5 G protein beta subunit (Gbeta5) controls the interaction of regulator of G protein signaling 9 (RGS9) with membrane anchors
Gbeta5's function in vision is reviewed.
under certain conditions, RGS9 and Gbeta5 may possibly function as betagamma dimer
From yeast two hybrid screening with HBX as bait, human guanine nucleotide binding protein beta subunit 5L (GNbeta5) was isolated from the cDNA library constructed in this study as a new hepatitis b X protein-interacting protein.
cytoplasmic RGS7*Gbeta5*R7BP heterotrimers and RGS7*Gbeta5 heterodimers are equivalently inefficient regulators of G protein-coupled receptor signaling relative to plasma membrane-bound heterotrimers bearing palmitoylated R7BP.
G-protein beta5 short splice variant isoform is indispensable for outer plexiform layer integrity and normal light responses of the retina in transgenic mice.
cytosolic chaperonin complex-dependent mechanism exists for Gbeta5-RGS7 assembly that utilizes the co-chaperone activity of PhLP1 in a unique way.
Stimulation of the ERK pathway in Gnb5(-/-) cells by epidermal growth factor restored M3R-stimulated insulin release to near normal levels. Identification of the novel role of Gbeta5-R7 in insulin secretion may lead to a new therapeutic approach for improving pancreatic beta-cell function
The complex of G protein regulator RGS9-2 and Gbeta(5) controls sensitization and signaling kinetics of type 5 adenylyl cyclase in the striatum.
Expression of the Gbeta5/R7-RGS protein complex in pituitary and pancreatic islet cells.
Gbeta5/RGS6 (guanine nucleotide binding protein beta5/regulator of G-protein signaling 6) complex modulates timing of parasympathetic influence on atrial myocytes and heart rate.
Elimination of Gbeta5-RGS complexes led to a striking level of hyperactivity that far exceeds activity levels previously observed in animal models.
We conclude that even a partial reduction in Gbeta5-R7 level can perturb normal animal metabolism and behavior.
Gbeta5 regulates dendritic arborization and/or synapse formation during development, in part by effects on gene expression; mice lacking Gbeta5 have a markedly abnormal neurologic phenotype.
regulator of G-protein signalling 7 binding protein contributes significantly to the nuclear localization of endogenous G beta(5)/R7-RGS complex in brain
study found that RGS7-Gbeta5 complexes bound to G protein-gated potassium channels and facilitated their functional coupling to GABA(B) receptors in neurons
Disruption of the Gbeta5 gene in mice abolishes expression of Gbeta5-L in the retina and also greatly reduces the expression level of RGS9-1, indicating a complex containing RGS9-1-Gbeta5-L is essential for normal G-protein deactivation and rod function
photoreceptors R9AP determines the stability of the RGS9.Gbeta5 complex, and therefore all three proteins, RGS9, Gbeta5 , and R9AP, are obligate members of the regulatory complex that speeds the rate at which transducin hydrolyzes GTP.
G-protein beta5 short splice variant isoform is indispensable for outer plexiform layer integrity and normal light responses of the retina.
R7-Gbeta5-R7BP complexes in the mouse could regulate signaling by modulatory Gi/o-coupled GPCRs in the developing and adult nervous systems.
Delivery of RGS7/Gbeta5 to dendrites of ON-bipolar cells occurs independently of its association with R7BP. These findings provide a new mechanism for adapter-independent targeting of RGS/Gbeta5 complexes.
Gbeta5 and R7BP in striatum undergo remodeling upon changes in neuronal activity.
Heterotrimeric guanine nucleotide-binding proteins (G proteins), which integrate signals between receptors and effector proteins, are composed of an alpha, a beta, and a gamma subunit. These subunits are encoded by families of related genes. This gene encodes a beta subunit. Beta subunits are important regulators of alpha subunits, as well as of certain signal transduction receptors and effectors. Alternatively spliced transcript variants encoding different isoforms exist.
G protein, beta subunit 5L
, G protein, beta-5 subunit
, guanine nucleotide-binding protein subunit beta-5
, guanine nucleotide-binding protein, beta subunit 5L
, transducin beta chain 5
, guanine nucleotide binding protein, beta 5
, guanine nucleotide binding protein (G protein), beta polypeptide 5
, guanine nucleotide-binding protein, beta-5 subunit
, guanine nucleotide binding protein beta 5