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Molecular and Cellular Biology, June 2002, p. 4094-4100, Vol. 22, No. 12
0270-7306/02/$04.00+0     DOI: 10.1128/MCB.22.12.4094-4100.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

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

Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland 20852,¹ Division of Hematologic Products, Center for Biological Evaluation and Research, Food and Drug Administration, Bethesda, Maryland 20892,² Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York 10461³

Received 20 November 2001/ Returned for modification 17 March 2002/ Accepted 14 March 2002

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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