期刊
MOLECULAR AND CELLULAR BIOLOGY
卷 21, 期 24, 页码 8365-8370出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.21.24.8365-8370.2001
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资金
- NIAID NIH HHS [AI 41082] Funding Source: Medline
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.
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