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> | |||
==Pharmacogenomics== | ==Pharmacogenomics== | ||
Regarding the treatment of heart failure, there is conflicting evidence whether [[beta-blocker]]s are as effective in African-American patients as in Anglo patients.<ref name="pmid12742294">{{cite journal |author=Shekelle PG, Rich MW, Morton SC, ''et al'' |title=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 |journal=J. Am. Coll. Cardiol. |volume=41 |issue=9 |pages=1529–38 |year=2003 |pmid=12742294 |doi=}}</ref> This may be due to a polymorphism in African-American patients of the G protein–coupled [[cell surface receptor]] kinase (GRK5) ([http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=600870 OMIM]) that confers a natural "genetic beta-blockade".<ref name="doi10.1038/nm1750">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).</ref> | Regarding the treatment of [[heart failure]], there is conflicting evidence whether [[beta-blocker]]s [[medication]]s are as effective in African-American patients as in Anglo patients.<ref name="pmid12742294">{{cite journal |author=Shekelle PG, Rich MW, Morton SC, ''et al'' |title=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 |journal=J. Am. Coll. Cardiol. |volume=41 |issue=9 |pages=1529–38 |year=2003 |pmid=12742294 |doi=}}</ref> This may be due to a polymorphism in African-American patients of the G protein–coupled [[cell surface receptor]] kinase (GRK5) ([http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=600870 OMIM]) that confers a natural "genetic beta-blockade".<ref name="doi10.1038/nm1750">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).</ref> | ||
==References== | |||
<references/> | |||
Revision as of 08:25, 6 January 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]
Pharmacogenomics
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.[2] 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".[3]
References
- ↑ Anonymous (2024), G-protein-coupled receptor kinase (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).