Apoptosis-Linked Gene 2-Deficient Mice Exhibit Normal T-Cell Development and Function

AUTOR(ES)

Jang, Ihn Kyung

FONTE

American Society for Microbiology

RESUMO

The apoptosis-linked gene product, ALG-2, is a member of the family of intracellular Ca2+-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.

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