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Atypical Actions of G Protein-Coupled Receptor Kinases
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  • Atypical Actions of G Protein-Coupled Receptor Kinases
  • Atypical Actions of G Protein-Coupled Receptor Kinases
저자명
Kurose. Hitoshi
간행물명
Biomolecules & therapeutics
권/호정보
2011년|19권 4호|pp.390-397 (8 pages)
발행정보
한국응용약물학회
파일정보
정기간행물|ENG|
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
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기타언어초록

G protein-coupled receptor kinases (GRKs) and ${eta}$-arrestins have been known as regulators of G protein-coupled receptors. However, it has been recently reported that GRKs and ${eta}$-arrestins mediate receptor-mediated cellular responses in a G proteinin-dependent manner. In this scheme, GRKs work as a mediator or a scaffold protein. Among 7 members of the GRK family (GRK1-GRK7), GRK2 is the most extensively studied in vitro and in vivo. GRK2 is involved in cellular migration, insulin signaling, and cardiovascular disease. GRK6 in concert with ${eta}$-arrestin 2 mediates chemoattractant-stimulated chemotaxis of T and B lymphocytes. GRK5 shuttles between the cytosol and nucleus, and regulates the activities of transcription factors. GRK3 and GRK4 do not seem to have striking effects on cellular responses other than receptor regulation. GRK1 and GRK7 play specific roles in regulation of rhodopsin function. In this review, these newly discovered functions of GRKs are briefly described.