-
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.
-
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.
-
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.
-
WDR26 is a novel Gbetagamma-binding protein that is required for the efficacy of Gbetagamma signaling and leukocyte migration
-
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).
