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anti-Human GNAQ Antibodies:
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Chicken Monoclonal GNAQ Primary Antibody for IF, WB - ABIN968914
Dutt, Kjoller, Giel, Hall, Toksoz: Activated Galphaq family members induce Rho GTPase activation and Rho-dependent actin filament assembly. in FEBS letters 2002
Show all 3 Pubmed References
Chicken Monoclonal GNAQ Primary Antibody for IF, WB - ABIN968915
Li, Iyengar: Calpain as an effector of the Gq signaling pathway for inhibition of Wnt/beta -catenin-regulated cell proliferation. in Proceedings of the National Academy of Sciences of the United States of America 2002
Show all 3 Pubmed References
Human Polyclonal GNAQ Primary Antibody for ELISA, WB - ABIN4315225
Ngai, Inngjerdingen, Berge, Taskén: Interplay between the heterotrimeric G-protein subunits Galphaq and Galphai2 sets the threshold for chemotaxis and TCR activation. in BMC immunology 2009
Human Monoclonal GNAQ Primary Antibody for ELISA, WB - ABIN516106
Sánchez-Fernández, Cabezudo, Caballero, García-Hoz, Tall, Klett, Michnick, Mayor, Ribas: Protein Kinase C ζ Interacts with a Novel Binding Region of Gαq to Act as a Functional Effector. in The Journal of biological chemistry 2016
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 Antibodies) expression and presence of the BRAF (show BRAF Antibodies) V600E mutation.
Mutations in GNAQ and GNA11 (show GNA11 Antibodies) 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 Antibodies)-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 Antibodies)/CLEC2R signaling is dependent on thromboxane A2 generation and is potentiated by co-stimulation with different GNAQ agonists. (CLEC2 (show CLEC1B Antibodies) = C-type lectin (show MBL2 Antibodies) CLEC2 (show CLEC1B Antibodies); CLEC2R = CLEC2 (show CLEC1B Antibodies) receptor; GNAQ = guanine nucleotide-binding protein (show COASY Antibodies) G[q] subunit alpha)
The findings of the work indicate a role for Galphaq and/or Galpha14 and in CCR2a/CCR2b (show CCR2 Antibodies)-stimulated Rho A (show RHOA Antibodies) GTPase (show RACGAP1 Antibodies)-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 Antibodies) expression. Combined GNAQ/11 and YAP (show YAP1 Antibodies) may constitute a putative precursor tumour pathway with an activated oncogene (show RAB1A Antibodies) (GNAQ/11) and downstream effector (YAP (show YAP1 Antibodies)).
RasGRP3 (show RASGRP3 Antibodies) mediates ERK MAPK (show MAPK1 Antibodies) pathway activation in GNAQ mutant uveal melanoma.
Galphaq regulates the development of rheumatoid arthritis by modulating Th1 (show TH1L Antibodies) differentiation
The GC/GC (show GC Antibodies) genotype of the TT(-695/-694)GC polymorphism is associated with increased Gq protein expression, augmented angiotensin II receptor type 1 (show AGTR1 Antibodies)-related vasoconstriction, and increased myocardial injury after coronary artery bypass grafting.
The Galphas (show GNAS Antibodies) and Galphaq peptides adopt different orientations in beta2-AR and V1AR (show AVPR1A Antibodies), respectively. The beta2-AR/Galphas (show GNAS Antibodies) peptide interface is dominated by electrostatic interactions, whereas the V1AR (show AVPR1A Antibodies)/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 Antibodies) in complex with Galphaq and Gbetagamma, in which the activated Galpha (show SUCLG1 Antibodies) subunit of Gq is fully dissociated from Gbetagamma and dramatically reoriented from its position in the inactive Galphabetagamma heterotrimer [g alphaq]
the impaired working memory in forebrain-specific Perk (show EIF2AK3 Antibodies) knockout mice may stem from altered Gq protein-coupled intracellular Ca(2 (show CA2 Antibodies)+) dynamics in cortical pyramidal neurons.
Galphaq regulates the development of rheumatoid arthritis by modulating Th1 (show HAND1 Antibodies) differentiation
Fluid shear stress acts on the Galphaq-ERK5 (show MAPK7 Antibodies) signaling pathway to upregulate Cyclin B1 (show CCNB1 Antibodies) and CDK1 (show CDK1 Antibodies) expression, thereby resulting in MC3T3-E1 cell proliferation.
activation of the Gq-membrane-associated estrogen receptors rapidly stimulates hypothalamic paraventricular nucleus CRH (show CRH Antibodies) 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 Antibodies), interacted with Galpha(q) and interfered with signaling through this G protein. These data support the development of GRK2 (show ADRBK1 Antibodies)-based therapeutic approaches to prevent hypertrophy and heart failure.
Galphaq/Galpha11 signaling pathways play a pivotal role in gene activity patterns during cardiac remodeling.
Developmental AHR activation by pollutants, and other exogenous ligands, increases the likelihood that Gnaq knockout mice will develop autoimmune diseases later in life.
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