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Logo of jbcThe Journal of Biological Chemistry
J Biol Chem. 2016 January 22; 291(4): 1564.
PMCID: PMC4722439

Figuring Out How the Nucleotide Receptor P2Y2R Regulates Expression of a Key Coagulation Factor

Purinergic P2Y2 Receptor Control of Tissue Factor Transcription in Human Coronary Artery Endothelial Cells. New AP-1 Transcription Factor Site and Negative Regulator

See referenced article, J. Biol. Chem. 2016, 291, 1553–1563

The P2Y2 receptor (P2Y2R) is a nucleotide receptor that is predominantly expressed in human coronary artery endothelial cells. ATP and UTP both activate P2Y2R to cause an increase in expression of tissue factor (TF). TF is involved in initiating the coagulation cascade. Overexpression of tissue factor causes strokes and heart attacks and the formation of plaque. The details of the mechanism of TF up-regulation through P2Y2R are unclear. In this Paper of the Week, a team led by Jianzhong Shen at Auburn University used bioinformatics tools and experimental assays to identify a site in the promoter for the TF gene-mediated transcription triggered by P2Y2R. The investigators also found a repressor called Fra-1 that down-regulated P2Y2R-induced tissue factor up-regulation. Based on their findings, the authors suggest “targeting the P2Y2R-Fra-1-TF pathway may be an attractive new strategy for controlling vascular inflammation and thrombogenicity associated with endothelial dysfunction.”

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A systematic diagram showing a new two-way fine-tuning mechanism underlying P2Y2R-controlled cell signaling, promoter activation, and TF gene transcription in human coronary artery endothelial cells.

Articles from The Journal of Biological Chemistry are provided here courtesy of American Society for Biochemistry and Molecular Biology