|TDAG51 is not essential for Fas/CD95 regulation and apoptosis in vivo.
|Year of Publication
|Rho J, Gong S, Kim N, Choi Y
|Mol Cell Biol
|Animals, Apoptosis, Blotting, Northern, Cell Division, Concanavalin A, DNA, Complementary, Dose-Response Relationship, Drug, fas Receptor, Flow Cytometry, Lipopolysaccharides, Mice, Mice, Transgenic, Models, Genetic, Protein Binding, Reverse Transcriptase Polymerase Chain Reaction, T-Lymphocytes, Transcription Factors, Up-Regulation
Fas/CD95 is a key regulator of apoptotic signaling, which is crucial for the maintenance of homeostasis in peripheral lymphoid organs. TDAG51 has been shown to play critical roles in the up-regulation of Fas gene expression and T-cell apoptosis in vitro. In order to identify the role of TDAG51 in vivo, we generated TDAG51-deficient (TDAG51-/-) mice. Northern blotting revealed no expression of TDAG51 in TDAG51-/- mice, indicating that the TDAG51 gene was successfully targeted. TDAG51-/- mice were healthy and showed no gross developmental abnormalities. While Fas-deficient mice display marked lymphadenopathy, splenomegaly, and lymphocytosis, TDAG51-/- mice had no apparent defects in secondary lymphoid organs. Although TDAG51 is required for up-regulation of Fas expression in T-cell hybridomas, TDAG51-/- mice expressed normal levels of Fas and had normal T-cell apoptosis. Therefore, we conclude that TDAG51 is not essential for Fas up-regulation and T-cell apoptosis in vivo. There are several known homologs of TDAG51, and these homologs may substitute for TDAG51 in TDAG51-/- mice.
|Mol. Cell. Biol.
|PubMed Central ID
|AI 41082 / AI / NIAID NIH HHS / United States