MTOR-dependent synthesis of Bcl-3 controls the retraction of fibrin clots by activated human platelets.

ABSTRACT: New activities of human platelets continue to emerge. One unexpected response is new synthesis of proteins from previously transcribed RNAs in response to activating signals. We previously reported that activated human platelets synthesize B-cell lymphoma-3 (Bcl-3) under translational control by mammalian target of rapamycin (mTOR). Characterization of the ontogeny and distribution of the mTOR signaling pathway in CD34+ stem cell-derived megakaryocytes now demonstrates that they transfer this regulatory system to developing proplatelets. We also found that Bcl-3 is required for condensation of fibrin by activated platelets, demonstrating functional significance for mTOR-regulated synthesis of the protein. Inhibition of mTOR by rapamycin blocks clot retraction by human platelets. Platelets

SUBMITTER: Weyrich AS 

PROVIDER: S-EPMC1801071 | biostudies-literature | 2007 Mar

REPOSITORIES: biostudies-literature