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Validated All-in-One™ qPCR Primer for GRK5(NM_005308.2) Search again
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:
Summary
This gene encodes a member of the guanine nucleotide-binding protein (G protein)-coupled receptor kinase subfamily of the Ser/Thr protein kinase family. The protein phosphorylates the activated forms of G protein-coupled receptors thus initiating their deactivation. It has also been shown to play a role in regulating the motility of polymorphonuclear leukocytes (PMNs). [provided by RefSeq].
Gene References into function
- Human substance P receptor undergoes agonist-dependent phosphorylation by G protein-coupled receptor kinase 5 in vitro.
- Data indicate that GRK5 does not regulate the sorting of human beta 2-adrenoceptors in the endocytic pathway.
- a group of hydrophobic amino acids within the membrane binding motif is critical to mediating the PM localization of GRK5
- GRK5 has a DNA-binding nuclear localization sequence
- High expression was detected in septic neutrophils and control cells treated with cytokines plus LPS.
- Results show that GRK5 plays a distinctive role in the phosphorylation of the beta2AR.
- GRK5-Leu41 represents a gain-of-function polymorphism that evokes enhanced loss-of-function of beta2AR during persistent agonist exposure, and thus may contribute to beta-agonist variability in asthma treatment of African-Americans.
- Protective effect of a GRK5 polymorphism on heart failure and its interaction with beta-adrenergic receptor antagonists is reported.
- GRK5 overexpression causes nuclear accumulation of IkappaB alpha, leading to the inhibition of NFkappaB transcriptional activity.
- Reciprocity of regulation between platelet-derived growth factor receptor beta (PDGFRbeta) and GRK5, or their activation/deactivation cycle, mirrors other reciprocal regulatory mechanisms affecting tyrosine kinases.
