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Validated All-in-One™ qPCR Primer for GNAQ(NM_002072.4) Search again
Product ID:
HQP007754
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CMAL, CMC1, G-ALPHA-q, GAQ, SWS
Gene Description:
G protein subunit alpha q
Target Gene Accession:
NM_002072.4(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
Guanine nucleotide-binding proteins are a family of heterotrimeric proteins that couple cell surface, 7-transmembrane domain receptors to intracellular signaling pathways. Receptor activation catalyzes the exchange of GTP for GDP bound to the inactive G protein alpha subunit resulting in a conformational change and dissociation of the complex. The G protein alpha and beta-gamma subunits are capable of regulating various cellular effectors. Activation is terminated by a GTPase intrinsic to the G-alpha subunit. G-alpha-q is the alpha subunit of one of the heterotrimeric GTP-binding proteins that mediates stimulation of phospholipase C-beta (MIM 600230).[supplied by OMIM].
Gene References into function
- The increase in Gqalpha and Gialpha1/2 expression was accompanied by an increase in Ca2+ signaling triggered by thrombin and other agonists known to signal to Ca2+ via these G-proteins in platelets.
- A hemorrhagic diathesis patient has a defect in Galphaq gene expression in platelets but not neutrophils, possibly due to defects in transcriptional regulation or mRNA stability, and suggest a hematopoietic-lineage specific defect.
- existence of a novel molecular mechanism by which Galpha(q) and the large family of G(q)-coupled receptors can regulate the activity of Rho and its downstream signaling pathways
- regulation of signaling by ezrin-radixin-moesin-binding phosphoprotein-50
- Galpha protein signaling can lead to internalization of GPCRs, with specificity in both the Galpha proteins and GPCRs that are involved
- Gq/11 proteins mediate KDR tyrosine phosphorylation and KDR-mediated HUVEC proliferation through interaction with KDR.
- agonist binding to Gq-coupled receptors blocks Akt activation via the release of active Galphaq subunits that inhibit phosphatidylinositol 3-kinase
- The rapid, shear-induced activation of Ras is mediated by Galpha(q) through the activity of Gbetagamma subunits in human vascular endothelial cells.
- G protein-coupled receptors might evoke G alpha and G beta gamma to orchestrate regulation of phospholipase signaling by tubulin dimers and control of cell shape by microtubules
- Gq-coupled receptors activate glycogen synthase kinase-3beta and C-terminal Src kinase
- G alpha q and platelet activating factor receptor lead to stimulation of Src and focal adhesion kinase in vascular endothelium
- the co-operative effect between Gbetagamma-mediated signaling and the increased intracellular Ca(2+) level represents a robust mechanism for the stimulation of JNK by G(q)-coupled receptors
- (HEK) 293 cells expressing recombinant Galpha(q/11)-coupled muscarinic M3 receptors showed transient coexpression of RGS proteins
- PC1 signaling elevates intracellular Ca(2+), activates Galpha(q) and PLC, which then activates calcineurin and NFAT
- analysis of the GRK2 binding site of Galphaq
- beta-Arrestin 1 and Galphaq/11 have roles in activating RhoA and stress fiber formation following receptor stimulation
- These data indicate that the preserved integrity of plasma membrane domains/caveolae is required for complete agonist-induced phosphorylation of G(q)/G(11)alpha.
- PKC epsilon and delta are the main PKC isozymes involved in G alpha(q)-mediated signaling in human atria
- Galphaq potentiation of AC9 activity involves Ca2+/calmodulin and CaMKII.
- Alpha-betagamma binding is necessary at a point downstream from receptor activation of the heterotrimeric G protein for signal transduction by alpha q.
- Results suggest that the G(q) class proteins are degraded through the proteasome pathway and that cellular localization and/or other protein interactions determine their stability.
- Quantitative analysis indicated that Galpha(q/11) subunits are abundant polypeptides in human brain, with values ranging from about 1200 ng/mg in cerebral cortex to close to 900 ng/mg of membrane protein in caudate
- Our results support a novel model where activated Galpha(q) forms molecular complexes with ARNO and ARF6, possibly through a direct interaction with ARNO, leading to ARF6 activation.
- alternative pathway operates in the absence of Lck-dependent tyrosine-phosphorylation events and was initiated by the T cell receptor-dependent activation of raft-enriched heterotrimeric Galpha11 proteins
- Contractile dysfunction and pathological structural changes in the myocardium of Galpha(q) transgenic mice improve significantly after termination of the Galpha(q) signal, even in animals with overt heart failure.
- GTP-Binding Protein alpha Subunits, Gq-G11, gene is regulated during megakaryocytic differentiation by early growth response 1 transcription factor.
- Galphaq activation of TRPC6 signals the activation of PKCalpha, and thereby induces RhoA activity and endothelial cell contraction
- These lines of evidence suggested that a Gq-coupled receptor activates specifically p38 MAPK through lipid rafts and Src kinase activation, in which flotillins positively modulate the Gq signaling.
- two distinct regions of the Cav3.3 channel are necessary and sufficient for complete M1 receptor-mediated channel inhibition
- Solubilization of this class of Galpha proteins was observed after prolonged agonist stimulation, induced by ultra high concentration of hormone and in cells expressing a large number of GPCRs, revealing tight binding of G(q)alpha protein to the membrane
- Galphaq directly activates p63RhoGEF and Trio via a conserved extension of the Dbl homology-associated pleckstrin homology domain
- Polymorphism of the Galphaq gene is associated with accelerated mortality in heart failure
- the crystal structure of the Galphaq-p63RhoGEF-RhoA complex, detailing the interactions of Galphaq with the Dbl and pleckstrin homology (DH and PH) domains of p63RhoGEF was determined
- The M(1) receptor is the predominant mAChR subtype coupling to the Galpha(q/11) G protein in the cerebral cortex.
- A novel polymorphism in the Gq promoter region is associated with enhanced promoter activity, Gq expression, intracellular signal transduction, and increased prevalence of left ventricular hypertrophy, particularly in women.
- These novel data demonstrate an IKK2-dependent, predominantly G-protein-independent pathway involved in PAR-2 regulation of NFkappaB phosphorylation in keratinocytes.
- We show that Env-mediated Rac-1 activation is dependent on the activation of Galpha(q) and its downstream targets.
- GNAQ mutations occur in about half of uveal melanomas, representing the most common known oncogenic mutation in this cancer.
- MLK3 functions in a regulated way to limit levels of the activated GTPase Rho by binding to the Rho activator, p63RhoGEF/GEFT, which, in turn, prevents its activation by Galphaq.
- Report phorbol 12-myristate 13-acetate responsive sequence in Galphaq promoter during megakaryocytic differentiation. Regulation by EGR-1 and MAP kinase pathway.
- a role of Galphaq in the fine-tuning of proximal TCR signals at the level of Lck and a negative regulatory role of Galphaq in transcriptional activation of cytokine responses.
- frequent somatic mutations in the heterotrimeric G protein alpha-subunit, GNAQ, in blue naevi (83%) and ocular melanoma of the uvea (46%)