Brief Reviews |
From the Biomedical Research Division, The University of Texas Health Center at Tyler, Tex.
Correspondence to L. Vijaya Mohan Rao, PhD, Biomedical Research, The University of Texas Health Center at Tyler, 11937 US Highway 271, Tyler, TX 75708. E-mail vijay.rao{at}uthct.edu
How does tissue factor (TF), whose principle role is to support clotting factor VIIa (FVIIa) in triggering the coagulation cascade, affect various pathophysiological processes? One of the answers is that TF interaction with FVIIa not only initiates clotting but also induces cell signaling via activation of G-proteincoupled protease activated receptors (PARs). Recent studies using various cell model systems and limited in vivo systems are beginning to define how TFVIIa-induced signaling regulates cellular behavior. Signaling pathways initiated by both TFVIIa protease activation of PARs and phosphorylation of the TFcytoplasmic domain appear to regulate cellular functions. In the present article, we review the emerging data on the mechanism of TF-mediated cell signaling and how it regulates various cellular responses, with particular focus on TFVIIa protease-dependent signaling.
Recent studies show that tissue factorfactor VIIa, whose primary function is to initiate the clotting cascade, transduces cell signaling in various cell types. This brief review summarizes recent literature on potential mechanisms by which tissue factorfactor VIIa activates cell signaling, and how tissue factorfactor VIIa-induced cell signaling may affect various pathophysiological processes.
Key Words: tissue factor factor VIIa protease activated receptors cell signaling
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