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Validated All-in-One™ qPCR Primer for GNA11(NM_002067.4) Search again
Product ID:
HQP007743
(click here to view gene annotation page)
Species:
Human
Symbol:
Alias:
FBH, FBH2, FHH2, GNA-11, HG1K, HHC2, HYPOC2
Gene Description:
G protein subunit alpha 11
Target Gene Accession:
NM_002067.4(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:
Gene References into function
- the C-terminal domain participates intimately in the efficacy of B1R and B2R G(q/11) coupling by contributing both positive and negative regulatory epitopes.
- GNA11 is involved in signalling of gonadotropin-releasing hormone receptor, which negatively regulates cell growth. Down-regulation is suggested to be involved in human breast cancers.
- a new signaling pathway by which G alpha(q/11)-coupled receptors specifically induce Rho signaling through a direct interaction of activated G alpha(q/11) subunits with p63RhoGEF.
- regulation of the PLC pathway through the PTH1R is significantly increased by elevating expression of G(11)alpha in osteoblastic cells.
- TPO integrates G(i), but not G(q), stimulation, supports integrin alpha(IIb)beta(3) activation platelet aggregation independently of phospholipase C but requires PI3-kinase and Rap1B
- These results indicate that the thio-acylation status of the alpha1b-adrenoceptor does not regulate G protein activation whereas thio-acylation of Galpha11 plays a key role in activation by the receptor.
- soluble amyloid precursor protein release enhancement induced by muscarinic receptor stimulation was decreased by a G(q/11) minigene construct
- CB(1) receptors are stabilized in a conformation that enables G(q)11 signaling by the WIN55212-2 cannabinoid agonist, thus shifting the G protein specificity of the receptor
- the ability of MAS to up-regulate AT(1) receptor levels reflects the constitutive capacity of MAS to activate Galpha(q)/Galpha(11) and hence stimulate PKC-dependent phosphorylation of the AT(1) receptor
- G(q/11)-coupled receptors are the principal G protein-coupled receptor subfamily mediating cooperative mitogenic signaling in airway smooth musscle.
- The phosphorylation of Galpha11 protein represents a novel mechanism involved in regulation of receptor 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(11)alpha protein to the membran
- Protein kinase C-related kinase and ROCK are required for thrombin-induced endothelial cell permeability downstream from Galpha12/13 and Galpha11/q
