| First Author | Jang IK | Year | 2002 |
| Journal | Mol Cell Biol | Volume | 22 |
| Issue | 12 | Pages | 4094-100 |
| PubMed ID | 12024023 | Mgi Jnum | J:76789 |
| Mgi Id | MGI:2180277 | Doi | 10.1128/MCB.22.12.4094-4100.2002 |
| Citation | Jang IK, et al. (2002) Apoptosis-linked gene 2-deficient mice exhibit normal T-cell development and function. Mol Cell Biol 22(12):4094-100 |
| abstractText | The apoptosis-linked gene product, ALG-2, is a member of the family of intracellular Ca(2+)-binding proteins and a part of the apoptotic machinery controlled by T-cell receptor (TCR), Fas, and glucocorticoid signals. To explore the physiologic function of ALG-2 in T-cell development and function, we generated mice harboring a null mutation in the alg-2 gene. The alg-2 null mutant mice were viable and fertile and showed neither gross developmental abnormality nor immune dysfunction. Analyses of apoptotic responses of ALG-2-deficient T cells demonstrated that ALG-2 deficiency failed to block apoptosis induced by TCR, Fas, or dexamethasone signals. These findings indicate that ALG-2 is physiologically dispensable for apoptotic responses induced by the above signaling pathways and suggest that other functionally redundant proteins might exist in mammalian cells. |
