G-protein-coupled receptor kinase: Difference between revisions
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In [[biochemistry]] and [[signal transduction]], '''G-protein-coupled receptor kinases''' are a "family of serine-threonine kinases that are specific for [[G-protein-coupled receptor]]s. They are regulatory proteins that play a role in [[G-protein-coupled receptor]] densensitization."<ref>{{MeSH}}</ref> | In [[biochemistry]] and [[signal transduction]], '''G-protein-coupled receptor kinases''' are a "family of serine-threonine kinases that are specific for [[G-protein-coupled receptor]]s. They are regulatory proteins that play a role in [[G-protein-coupled receptor]] densensitization."<ref>{{MeSH}}</ref> | ||
==Classification== | |||
* [[G-protein-coupled receptor kinase 1]] is "a protein-serine-threonine kinase that is found in photoreceptor cells. It mediates light-dependent phosphorylation of rhodopsin and plays an important role in phototransduction."<ref>{{MeSH|G-protein-coupled receptor kinase 1}}</ref> | |||
* beta-[[adrenergic receptor]] kinases | |||
** [[G-protein-coupled receptor kinase 2]] is "a ubiquitously expressed g-protein-coupled receptor kinase subtype that has specificity for the agonist-occupied form of beta-[[adrenergic receptor]]s. It may play an essential role in regulating myocardial contractile response."<ref>{{MeSH|G-protein-coupled receptor kinase 2}}</ref> | |||
** [[G-protein-coupled receptor kinase 3]] is "a ubiquitously expressed g-protein-coupled receptor kinase subtype that has specificity for the agonist-occupied form of beta-[[adrenergic receptor]]s and a variety of other g-protein-coupled-receptors. Although it is highly homologous to g-protein-coupled receptor kinase 2, it is not considered to play an essential role in regulating myocardial contractile response."<ref>{{MeSH|G-protein-coupled receptor kinase 3}}</ref> | |||
* [[G-protein-coupled receptor kinase 4]] is "a G-protein-coupled receptor kinase subtype that is primarily expressed in the [[testes]] and [[brain]]. Variants of this subtype exist due to multiple alternative splicing of its mRNA."<ref>{{MeSH|G-protein-coupled receptor kinase 4}}</ref> | |||
* [[G-protein-coupled receptor kinase 5]] is "a g-protein-coupled receptor kinase subtype that is primarily expressed in the myocardium and may play a role in the regulation of cardiac function."<ref>{{MeSH|G-protein-coupled receptor kinase 5}}</ref> | |||
==Pharmacogenomics== | ==Pharmacogenomics== | ||
Revision as of 08:58, 9 July 2009
In biochemistry and signal transduction, G-protein-coupled receptor kinases are a "family of serine-threonine kinases that are specific for G-protein-coupled receptors. They are regulatory proteins that play a role in G-protein-coupled receptor densensitization."[1]
Classification
- G-protein-coupled receptor kinase 1 is "a protein-serine-threonine kinase that is found in photoreceptor cells. It mediates light-dependent phosphorylation of rhodopsin and plays an important role in phototransduction."[2]
- beta-adrenergic receptor kinases
- G-protein-coupled receptor kinase 2 is "a ubiquitously expressed g-protein-coupled receptor kinase subtype that has specificity for the agonist-occupied form of beta-adrenergic receptors. It may play an essential role in regulating myocardial contractile response."[3]
- G-protein-coupled receptor kinase 3 is "a ubiquitously expressed g-protein-coupled receptor kinase subtype that has specificity for the agonist-occupied form of beta-adrenergic receptors and a variety of other g-protein-coupled-receptors. Although it is highly homologous to g-protein-coupled receptor kinase 2, it is not considered to play an essential role in regulating myocardial contractile response."[4]
- G-protein-coupled receptor kinase 4 is "a G-protein-coupled receptor kinase subtype that is primarily expressed in the testes and brain. Variants of this subtype exist due to multiple alternative splicing of its mRNA."[5]
- G-protein-coupled receptor kinase 5 is "a g-protein-coupled receptor kinase subtype that is primarily expressed in the myocardium and may play a role in the regulation of cardiac function."[6]
Pharmacogenomics
Heart failure
Regarding the treatment of heart failure, there is conflicting evidence whether beta-blockers medications are as effective in African-American patients as in Anglo patients.[7] This may be due to a polymorphism in African-American patients of the G protein–coupled cell surface receptor kinase (GRK5) (OMIM) that confers a natural "genetic beta-blockade".[8]
Asthma
Genetic polymorphisms may affect the response to adrenergic beta-antagonists by patients of African descent.[9]
References
- ↑ Anonymous (2024), G-protein-coupled receptor kinase (English). Medical Subject Headings. U.S. National Library of Medicine.
- ↑ Anonymous (2024), G-protein-coupled receptor kinase 1 (English). Medical Subject Headings. U.S. National Library of Medicine.
- ↑ Anonymous (2024), G-protein-coupled receptor kinase 2 (English). Medical Subject Headings. U.S. National Library of Medicine.
- ↑ Anonymous (2024), G-protein-coupled receptor kinase 3 (English). Medical Subject Headings. U.S. National Library of Medicine.
- ↑ Anonymous (2024), G-protein-coupled receptor kinase 4 (English). Medical Subject Headings. U.S. National Library of Medicine.
- ↑ Anonymous (2024), G-protein-coupled receptor kinase 5 (English). Medical Subject Headings. U.S. National Library of Medicine.
- ↑ Shekelle PG, Rich MW, Morton SC, et al (2003). "Efficacy of angiotensin-converting enzyme inhibitors and beta-blockers in the management of left ventricular systolic dysfunction according to race, gender, and diabetic status: a meta-analysis of major clinical trials". J. Am. Coll. Cardiol. 41 (9): 1529–38. PMID 12742294. [e]
- ↑ Liggett, Stephen B et al. 2008. A GRK5 polymorphism that inhibits [beta]-adrenergic receptor signaling is protective in heart failure. Nat Med advanced online publication. http://dx.doi.org/10.1038/nm1750 (Accessed April 29, 2008).
- ↑ Wang WC, Mihlbachler KA, Bleecker ER, Weiss ST, Liggett SB (August 2008). "A polymorphism of G-protein coupled receptor kinase5 alters agonist-promoted desensitization of beta2-adrenergic receptors". Pharmacogenet. Genomics 18 (8): 729–32. DOI:10.1097/FPC.0b013e32830967e9. PMID 18622265. Research Blogging.