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The novel angiotensin II type 1 receptor (AT1R)‐associated protein ATRAP downregulates AT1R and ameliorates cardiomyocyte hypertrophy
Author(s) -
Tanaka Yutaka,
Tamura Kouichi,
Koide Yuichi,
Sakai Masashi,
Tsurumi Yuko,
Noda Yoshihiro,
Umemura Masanari,
Ishigami Tomoaki,
Uchino Kazuaki,
Kimura Kazuo,
Horiuchi Masatsugu,
Umemura Satoshi
Publication year - 2005
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2005.01.068
Subject(s) - angiotensin ii , downregulation and upregulation , receptor , protein kinase a , medicine , endocrinology , muscle hypertrophy , phosphorylation , microbiology and biotechnology , chemistry , renin–angiotensin system , p38 mitogen activated protein kinases , angiotensin receptor , angiotensin ii receptor type 1 , kinase , biology , gene , biochemistry , blood pressure
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.