
pmid: 15757644
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.
Transcription, Genetic, Genetic Vectors, Down-Regulation, Cardiomegaly, Cardiomyocyte, Signal transduction, Transfection, p38 Mitogen-Activated Protein Kinases, Receptor, Angiotensin, Type 1, Adenoviridae, Mice, Animals, Immunoprecipitation, Myocytes, Cardiac, RNA, Messenger, Phosphorylation, Cells, Cultured, Adaptor Proteins, Signal Transducing, Cell Size, Angiotensin II, Hypertrophy, Angiotensin II type 1 receptor, Protein Biosynthesis, Downregulation, Proto-Oncogene Proteins c-fos
Transcription, Genetic, Genetic Vectors, Down-Regulation, Cardiomegaly, Cardiomyocyte, Signal transduction, Transfection, p38 Mitogen-Activated Protein Kinases, Receptor, Angiotensin, Type 1, Adenoviridae, Mice, Animals, Immunoprecipitation, Myocytes, Cardiac, RNA, Messenger, Phosphorylation, Cells, Cultured, Adaptor Proteins, Signal Transducing, Cell Size, Angiotensin II, Hypertrophy, Angiotensin II type 1 receptor, Protein Biosynthesis, Downregulation, Proto-Oncogene Proteins c-fos
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