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B‐Myb regulates the A~2B~ adenosine receptor in vascular smooth muscle cells by Cynthia St. Hilaire; Dan Yang; Barbara M. Schreiber; Katya Ravid is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

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## Abstract The A~2B~ adenosine receptor (A~2B~AR) has been described to control various vascular functions, including inhibition of smooth muscle cell proliferation. Here, we sought to understand the regulation of __A__~__2B__~__AR__ gene expression in aortic vascular smooth muscle cells (VSMCs), with a focus on the proliferation phase. Assays with A~2B~AR‐β‐gal aortic VSMCs, in which the endogenous __A__~__2B__~__AR__ gene promoter drives the expression of prokaryotic β‐galactosidase (β‐gal) instead of the endogenous __A__~__2B__~__AR__ gene, show that β‐gal expression is upregulated when the cells are induced to exit from cell cycle arrest. Similarly, the level of A~2B~AR mRNA is upregulated in proliferating primary aortic VSMCs. In search of related mechanisms, it was noted that the __A__~__2B__~__AR__ gene promoter contains several putative binding sites for the proliferation‐inducing transcription factor, B‐Myb. Using a clone of the 5′ region upstream of the mouse __A__~__2B__~__AR__ gene linked to a reporter gene, B‐Myb site deletion mutants were generated. It was determined that B‐Myb upregulates the __A__~__2B__~__AR__ gene promoter, and specific promoter binding sites wer

Who reads B‐Myb regulates the A~2B~ adenosine receptor in vascular smooth muscle cells?

Author

Cynthia St. Hilaire; Dan Yang; Barbara M. Schreiber; Katya Ravid

Publisher

John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley (ISSN 0730-2312)

Published

2007

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)