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Data, including data from studies using transgenic/knockout mice, suggest that Ppp1ca (zeige PPP1CA Proteine) and Gnb1 interact in quiescent platelets; then, Ppp1ca (zeige PPP1CA Proteine) and Plcb3 (zeige PLCB3 Proteine) interact during platelet aggregation; thus, Gnb1 enlists Ppp1ca (zeige PPP1CA Proteine) to modulate G protein-coupled receptor (zeige GPR34 Proteine) signaling. (Ppp1ca (zeige PPP1CA Proteine) = protein phosphatase 1 (zeige PPP1CB Proteine), catalytic subunit alpha; Gnb1 = guanine nucleotide-binding protein (zeige TRIM23 Proteine), subunit beta-1; Plcb3 (zeige PLCB3 Proteine) = phospholipase C (zeige PLC Proteine), subunit beta-3)
It was concluded that GIRK2 (zeige KCNJ6 Proteine), through its dual responsiveness to G protein beta (zeige GNB3 Proteine)-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 (zeige IGF1R Proteine)-Gbetagamma-phospho(T94)Tctex-1 (zeige DYNLT1 Proteine) signaling pathway promotes the proliferation of neural progenitors through modulation of ciliary resorption and G1 length.
ectopically expressed cTalpha (zeige PCYT1A Proteine) 1) forms a heterotrimeric complex with rod Gbeta (zeige SUCLG2 Proteine)(1)gamma(1), and substitutes equally for rTalpha in generating photoresponses initiated by either rhodopsin (zeige RHO Proteine) or S-cone opsin (zeige RHO Proteine)
Results suggest a model in which the Gbetagamma dimer that is released as a result of the dissociation from Galpha(o (zeige GNAO1 Proteine)) upon activation of mGluR6 (zeige GRM6 Proteine) closes the TRPM1 (zeige TRPM1 Proteine) channel, perhaps via a direct interaction.
WDR26 (zeige WDR26 Proteine) 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
G betagamma binds HDAC5 (zeige HDAC5 Proteine) and inhibits its transcriptional co-repression activity
G protein betagamma subunits stimulate type V and VI adenylyl cyclases
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 (zeige SUCLG2 Proteine) fold, disrupting interactions with CCT (zeige FLVCR2 Proteine) and releasing a PhLP1-Gbeta (zeige SUCLG2 Proteine) 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 (zeige FRAP1 Proteine) interacts with Gbetagamma.
GNB1 plays an important role in the mTOR (zeige FRAP1 Proteine)-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 (zeige NMUR1 Proteine) activation in cells including the angiotensin II type 1 receptor (zeige AGTR1 Proteine).
This study provided evidence that GNB1 gene polymorphisms are related to rapid virological response in HCV-1 and HCV-2 (zeige BMPER Proteine) infected patients. GNB1 may play an important role in activating the antiviral response prior to treatment.
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 (zeige RHO Proteine) and light-activated heterotrimeric transducin (zeige GNAT1 Proteine) (T-alpha-1, Gnb1, Gngt1 (zeige GNGT1 Proteine)); 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 (zeige ADRBK1 Proteine)-Gbeta1gamma2 complex is therefore most likely caused by specific interactions between PIP2 and the GRK2 (zeige ADRBK1 Proteine) 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