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Data, including data from studies using transgenic/knockout mice, suggest that Ppp1ca and Gnb1 interact in quiescent platelets; then, Ppp1ca and Plcb3 interact during platelet aggregation; thus, Gnb1 enlists Ppp1ca to modulate G protein-coupled receptor signaling. (Ppp1ca = protein phosphatase 1, catalytic subunit alpha; Gnb1 = guanine nucleotide-binding protein, subunit beta-1; Plcb3 = phospholipase C, subunit beta-3)
It was concluded that GIRK2, through its dual responsiveness to G protein beta-gamma and Na+, mediates a form of neuronal inhibition that is amplifiable in the setting of excess electrical activity.
During corticogenesis, a cilium-transduced, noncanonical IGF-1R-Gbetagamma-phospho(T94)Tctex-1 signaling pathway promotes the proliferation of neural progenitors through modulation of ciliary resorption and G1 length.
Data indicate that a decrease in the Gbeta1 production in Ggamma1 knockout rods resulted in a significant reduction in proteasomal overload and caused a striking reversal of photoreceptor degeneration.
ectopically expressed cTalpha 1) forms a heterotrimeric complex with rod Gbeta(1)gamma(1), and substitutes equally for rTalpha in generating photoresponses initiated by either rhodopsin or S-cone opsin
Results suggest a model in which the Gbetagamma dimer that is released as a result of the dissociation from Galpha(o) upon activation of mGluR6 closes the TRPM1 channel, perhaps via a direct interaction.
WDR26 is a novel Gbetagamma-binding protein that is required for the efficacy of Gbetagamma signaling and leukocyte migration
Our data suggest that the G-protein beta(1)gamma(2) dimer may play an important regulatory role in skeletal muscle excitation-contraction coupling.
G protein subunits beta1 and beta2 have different roles in neutrophil function, as revealed by gene expression silencing in primary mouse neutrophils
Gbeta1 is required for normal embryonic neurogenesis.
G betagamma binds HDAC5 and inhibits its transcriptional co-repression activity
G protein betagamma subunits stimulate type V and VI adenylyl cyclases
signaling pathway by which G(i)-coupled receptor specifically induces Rac and Cdc42 activation through direct interaction of Gbetagamma with FLJ00018.
Gbeta1 is the predominant Gbeta subunit expressed in olfactory sensory neurons.
Gbeta1-mediated Fyn activation integrates FAK with AJ, preventing persistent endothelial barrier leakiness.
Mutation in the GNB1 gene is associated with neurodevelopmental disorder and cutaneous mastocytosis.
Through analysis of the genomic and proteomic profiles of resistant cells, we identified an acquired mutation in the GNB1 gene, K89M, as the most likely cause of the resistance
Germline De Novo Mutations in GNB1 Cause Severe Neurodevelopmental Disability, Hypotonia, and Seizures.
we demonstrate a pathogenic role of de novo and autosomal dominant mutations in GNB1 as a cause of Global developmental delay and provide insights how perturbation in heterotrimeric G protein function contributes to the disease
PhLP1 binding stabilizes the Gbeta fold, disrupting interactions with CCT and releasing a PhLP1-Gbeta dimer for assembly with Ggamma.
GNB1 and GNB2 alterations confer transformed and resistance phenotypes across a range of human tumors and may be targetable with inhibitors of G protein signaling.
Data indicate that endogenous mTOR interacts with Gbetagamma.
GNB1 plays an important role in the mTOR-related anti-apoptosis pathway and can potentially be targeted in the treatment of human breast cancer.
Findings suggest a wide-ranging mechanism by which direct interaction of Gbetagamma with specific chromatin bound transcription factors regulates functional gene networks in response to GPCR activation in cells including the angiotensin II type 1 receptor.
This study provided evidence that GNB1 gene polymorphisms are related to rapid virological response in HCV-1 and HCV-2 infected patients. GNB1 may play an important role in activating the antiviral response prior to treatment.
Gbetagamma inhibits Epac-induced Ca 2+ elevation in melanoma cells. Cross talk of Ca 2+ signaling between Gbetagamma & Epac plays a major role in melanoma cell migration.
Data implicate the domain I-II linker region as an important contributor to voltage dependent Gbeta1/Ggamma2 modulation of Cav2.2 calcium channels.
This protein has been found differentially expressed in the anterior cingulate cortex from patients with schizophrenia
Data show that activation of PLCbeta(2) by alpha(q) and beta1gamma2 differ from activation by Rac2 and from each other.
Gbetagamma subunits enter in a protein complex with activated Rap1a and its effector Radil; this complex is required downstream of receptor stimulation for the activation of integrins and the positive modulation of cell-matrix adhesiveness.
Directional sensing requires GNB1-mediated PAK1 and PIX alpha-dependent activation of Cdc42.
Data show that G protein inhibition of N-type calcium channels is critically dependent on two separate but adjacent approximately 20-amino acid regions of the Gbeta subunit, as examined with Gbetas 1 and 5 and Ggamma2.
in elderly subjects of similar ages, those with diabetes have 1.7-fold higher levels of Galpha(i2) and twofold higher levels of Gbeta(1).
Gbeta1gamma2-mediated epithelial sodium channel (ENaC) inhibition involves activation of phospholipase C-beta and its enzymatic products that induce protein kinase C and ERK1/2 signaling pathways.
Data suggest that a hetero-multimer complex forms between light-activated rhodopsin and light-activated heterotrimeric transducin (T-alpha-1, Gnb1, Gngt1); the stoichiometry is 1:1 rhodopsin:transducin. The complex appears to form on native rod outer segment membranes upon light activation.
The PIP2-induced orientation of the GRK2-Gbeta1gamma2 complex is therefore most likely caused by specific interactions between PIP2 and the GRK2 PH domain.
determined the crystallographic structure of GRK2 in complex with G protein beta1gamma2 subunits
conclude that GNB1 constitutes over 99% of the GNbeta expressed in bovine rod outer segments and displays structural heterogeneity that is due to post-translational modification, some of which is due to phosphorylation of GNB1.
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. This gene uses alternative polyadenylation signals.
guanine nucleotide binding protein, beta 1
, guanine nucleotide-binding protein G(I)/G(S)/G(T) subunit beta-1
, transducin beta chain 1
, G protein, beta-1 subunit
, beta subunit, signal-transducing proteins GS/GI
, guanine nucleotide-binding protein G(I)/G(S)/G(T) beta subunit 1
, Guanine nucleotide-binding protein beta 1
, guanine nucleotide binding protein (G protein), beta 1
, guanine nucleotide-binding protein, beta-1 subunit
, rod transducin
, beta 1 subunit of heterotrimeric GTP-binding protein