Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10872804 | FEBS Letters | 2005 | 8 Pages |
Abstract
Activation of angiotensin II (Ang II) type 1 receptor (AT1R) signaling is reported to play an important role in cardiac hypertrophy. We previously cloned a novel molecule interacting with the AT1R, which we named ATRAP (for Ang II type 1 receptor-associated protein). Here, we report that overexpression of ATRAP significantly decreases the number of AT1R on the surface of cardiomyocytes, and also decreases the degree of p38 mitogen-activated protein kinase phosphorylation, the activity of the c-fos promoter and protein synthesis upon Ang II treatment. These results indicate that ATRAP significantly promotes downregulation of the AT1R and further attenuates certain Ang II-mediated hypertrophic responses in cardiomyocytes.
Keywords
SREAT1RAT2RAngiotensin II type 1 receptor-associated proteinPAGEERKATRAPACEPVDFp38MAPKJnkc-Jun N-terminal kinaseMAPKangiotensin II type 1 receptorAngiotensin-converting enzymeAngiotensin IIpolyacrylamide gel electrophoresisReverse transcriptaseC-terminalAng IIpolyvinylidene difluorideSerum response elementDownregulationCardiomyocyteSignal transductionHypertrophypolymerase chain reactionPCRmitogen-activated protein kinasep38 mitogen-activated protein kinaseExtracellular signal-regulated protein kinasecarboxy-terminalAngiotensin II type 2 receptor
Related Topics
Life Sciences
Agricultural and Biological Sciences
Plant Science
Authors
Yutaka Tanaka, Kouichi Tamura, Yuichi Koide, Masashi Sakai, Yuko Tsurumi, Yoshihiro Noda, Masanari Umemura, Tomoaki Ishigami, Kazuaki Uchino, Kazuo Kimura, Masatsugu Horiuchi, Satoshi Umemura,