Apoptosis-linked gene 2-deficient mice exhibit normal T-cell development and function

Ihn Kyung Jang, Renju Hu, Emanuela Lacaná, Luciano D'Adamio, Hua Gu

Research output: Contribution to journalArticle

53 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)4094-4100
Number of pages7
JournalMolecular and cellular biology
Volume22
Issue number12
DOIs
StatePublished - Jun 5 2002

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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