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Study demonstrated that the GNAQ p.R183Q mutation resides within endothelial cells in Sturge-Weber syndrome (SWS) brain lesions, and that the SWS brain endothelial cells can be isolated and expanded in culture and further confirm that the GNAQ p.R183Q mutation is present in brain endothelial cells.
Phospholipase C beta connects G protein signaling with RNA interference. (Review)
Adenocarcinomas or adenomas derived from pigmented ciliary epithelium is distinguished from uveal melanoma by the absence of SOX10 (show SOX10 ELISA Kits) expression and presence of the BRAF (show BRAF ELISA Kits) V600E mutation.
Mutations in GNAQ and GNA11 (show GNA11 ELISA Kits) genes in Greek uveal melanoma population present frequencies that qualify them as potential targets for customized therapy.
These results indicate that the mechanism by which Galphaq and PLC (show HSPG2 ELISA Kits)-beta3 mutually regulate each other is far more complex than a simple, two-state allosteric model and instead is probably kinetically determined.
Data (including data from studies using cells from knockout mice) suggest that CLEC2 (show CLEC1B ELISA Kits)/CLEC2R signaling is dependent on thromboxane A2 generation and is potentiated by co-stimulation with different GNAQ agonists. (CLEC2 (show CLEC1B ELISA Kits) = C-type lectin (show MBL2 ELISA Kits) CLEC2 (show CLEC1B ELISA Kits); CLEC2R = CLEC2 (show CLEC1B ELISA Kits) receptor; GNAQ = guanine nucleotide-binding protein (show COASY ELISA Kits) G[q] subunit alpha)
The findings of the work indicate a role for Galphaq and/or Galpha14 and in CCR2a/CCR2b (show CCR2 ELISA Kits)-stimulated Rho A (show RHOA ELISA Kits) GTPase (show RACGAP1 ELISA Kits)-mediated serum response factor activation.
GNAQ/11 mutant clones make up a fraction of the cells in choroidal nevi. Nevus cells are furthermore characterised by heterogeneous YAP (show YAP1 ELISA Kits) expression. Combined GNAQ/11 and YAP (show YAP1 ELISA Kits) may constitute a putative precursor tumour pathway with an activated oncogene (show RAB1A ELISA Kits) (GNAQ/11) and downstream effector (YAP (show YAP1 ELISA Kits)).
RasGRP3 (show RASGRP3 ELISA Kits) mediates ERK MAPK (show MAPK1 ELISA Kits) pathway activation in GNAQ mutant uveal melanoma.
Galphaq regulates the development of rheumatoid arthritis by modulating Th1 (show TH1L ELISA Kits) differentiation
The Galphas (show GNAS ELISA Kits) and Galphaq peptides adopt different orientations in beta2-AR and V1AR (show AVPR1A ELISA Kits), respectively. The beta2-AR/Galphas (show GNAS ELISA Kits) peptide interface is dominated by electrostatic interactions, whereas the V1AR (show AVPR1A ELISA Kits)/Galphaq peptide interactions are predominantly hydrophobic.
The phylogenetic trees reveal that porcine Gnaq, is evolutionarily close to the human homolog.
atomic structure of GRK2 (show ADRBK1 ELISA Kits) in complex with Galphaq and Gbetagamma, in which the activated Galpha (show SUCLG1 ELISA Kits) subunit of Gq is fully dissociated from Gbetagamma and dramatically reoriented from its position in the inactive Galphabetagamma heterotrimer [g alphaq]
results suggest that alveolar Gq/11 signaling maintains alveolar homeostasis and likely independently increases TGFbeta (show TGFB1 ELISA Kits) activation in response to the mechanical stress of the epithelium and decreases epithelial IL-33 (show IL33 ELISA Kits) synthesis. Together, these findings suggest that disruption of Gq/11 signaling promotes inflammatory emphysema but protects against mechanically induced lung injury.
the impaired working memory in forebrain-specific Perk (show EIF2AK3 ELISA Kits) knockout mice may stem from altered Gq protein-coupled intracellular Ca(2 (show CA2 ELISA Kits)+) dynamics in cortical pyramidal neurons.
Galphaq regulates the development of rheumatoid arthritis by modulating Th1 (show HAND1 ELISA Kits) differentiation
Fluid shear stress acts on the Galphaq-ERK5 (show MAPK7 ELISA Kits) signaling pathway to upregulate Cyclin B1 (show CCNB1 ELISA Kits) and CDK1 (show CDK1 ELISA Kits) expression, thereby resulting in MC3T3-E1 cell proliferation.
activation of the Gq-membrane-associated estrogen receptors rapidly stimulates hypothalamic paraventricular nucleus CRH (show CRH ELISA Kits) neurons by suppressing the M-current and potentiating glutamatergic neurotransmission
cell-penetrating peptides should effectively inhibit active Galphaq in cells and that these and genetically encoded sequences may find application as molecular probes, drug leads, and biosensors to monitor the spatiotemporal activation of Galphaq in cells.
the results have identified 138 and 150 ovarian genes that are up-regulated or down-regulated, respectively, at the end of gestation in a Galphaq/11-dependent fashion.
The betaARKrgs peptide, but not endogenous GRK2 (show ADRBK1 ELISA Kits), interacted with Galpha(q) and interfered with signaling through this G protein. These data support the development of GRK2 (show ADRBK1 ELISA Kits)-based therapeutic approaches to prevent hypertrophy and heart failure.
Galphaq/Galpha11 signaling pathways play a pivotal role in gene activity patterns during cardiac remodeling.
This locus encodes a guanine nucleotide-binding protein. The encoded protein, an alpha subunit in the Gq class, couples a seven-transmembrane domain receptor to activation of phospolipase C-beta. Mutations at this locus have been associated with problems in platelet activation and aggregation. A related pseudogene exists on chromosome 2.
, guanine nucleotide-binding protein G(q) subunit alpha
, guanine nucleotide-binding protein alpha-q
, G alpha q
, guanine nucleotide binding protein alpha q subunit
, guanine nucleotide binding protein, alpha q polypeptide
, guanine nucleotide regulatory protein G alpha q
, heterotrimeric guanine nucleotide-binding protein alpha q subunit
, guanine nucleotide-binding protein G(q) alpha subunit