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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adaptor Proteins, Signal Transducing / analysis
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Adaptor Proteins, Signal Transducing / genetics
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Adaptor Proteins, Signal Transducing / physiology*
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Adenoviridae / genetics
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Animals
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Cardiomegaly / genetics
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Cardiomegaly / metabolism
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Cell Size
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Cells, Cultured
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Down-Regulation*
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Genetic Vectors / genetics
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Hypertrophy
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Immunoprecipitation
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Mice
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Myocytes, Cardiac / chemistry
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Myocytes, Cardiac / cytology
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Myocytes, Cardiac / metabolism*
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Phosphorylation
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Protein Biosynthesis / genetics
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Protein Biosynthesis / physiology
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Proto-Oncogene Proteins c-fos / genetics
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Proto-Oncogene Proteins c-fos / metabolism
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RNA, Messenger / analysis
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RNA, Messenger / metabolism
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Receptor, Angiotensin, Type 1 / analysis
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Receptor, Angiotensin, Type 1 / genetics
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Receptor, Angiotensin, Type 1 / metabolism*
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Transcription, Genetic
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Transfection
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p38 Mitogen-Activated Protein Kinases / metabolism
Substances
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Adaptor Proteins, Signal Transducing
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Agtrap protein, mouse
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Proto-Oncogene Proteins c-fos
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RNA, Messenger
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Receptor, Angiotensin, Type 1
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p38 Mitogen-Activated Protein Kinases