Transactivation: a novel signaling pathway from angiotensin II to tyrosinekinase receptors

Authors
Citation
Y. Saito et Bc. Berk, Transactivation: a novel signaling pathway from angiotensin II to tyrosinekinase receptors, J MOL CEL C, 33(1), 2001, pp. 3-7
Citations number
33
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
ISSN journal
00222828 → ACNP
Volume
33
Issue
1
Year of publication
2001
Pages
3 - 7
Database
ISI
SICI code
0022-2828(200101)33:1<3:TANSPF>2.0.ZU;2-S
Abstract
Angiotensin II (Ang II), an octapeptide presser hormone, activates cellular events that may contribute to the pathogenesis of cardiovascular disease. The physiological actions of Ang II are mediated via the Ang II type I rece ptor (ATIR) and type 2 receptor (AT2R), which are G protein-coupled recepto rs (GPCR), GPCR share a common basic structure of seven transmembrane helic es connected by alternating cytoplasmic and extracellular Loops. GPCR lads intrinsic kinase activity possessed by receptor tyrosine kinases (RTK) such as platelet-derived growth factor receptor (PDGFR) or epidermal growth fac tor receptor (EGFR), Nonetheless, the signal transduction events activated by the AT1R mimic those of RTKs, Recently, cross-tail; between GPCR and RTK has been observed, There is accumulating evidence that GPCR take advantage of signaling pathways downstream of RTK to exert its effect on the cells. In this context, RTK may be considered as one of signaling molecules downst ream of GPCR. (C) 2000 Academic Press.