Bax and Bid act in synergy to bring about T11TS- mediated glioma apoptosis via the release of mitochondrial cytochrome c and subsequent caspase activation

摘要: The specific apoptotic role of T11TS has been well established in glioma animal models. specifically induces the cells to die an death via immune cross-talk with two intracranial competent cells-microglia and brain-infiltrating lymphocytes. To unearth molecular cascades operative within some extent interacting immunocytes, we had initiated studies where preliminary findings not only indicated involvement receptors but also hinted other regulators. Hence, identify pathway apoptosis involving regulators three cell types, were studied for intrinsic that engaged maintain mitochondrial membrane integrity. proteins selected could be divided into broad classes-the Bcl-2 family proteins-Bid, Bax Bcl-2; guardian genome p53 downstream mitochondria-Apaf-1, cytochrome c, caspase-9 caspase-3. Activated Bid as maximal expression was observed first dose thus dually activating pro-apoptotic second cells. Concurrently, pro-survival protein Bcl-2's level very much down-regulated same doses favoring internal microenvironment proceed apoptosis. High c Apaf-1 presence active caspase-3 all T11TS-treated tumor-bearing groups further adjudicated clear animals. Even though remained more or less indicating mitochondria intensity these lower than tumor present work focuses on mechanistic approach how mediates hence is its kind field immunology immunotherapeutic molecule's mode action worked out.