Apoptosis-linked gene 2-deficient mice exhibit normal T-cell development and function.
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.
Jang
Ihn Kyung
IK
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland 20852, USA.
Hu
Renju
R
Lacaná
Emanuela
E
D'Adamio
Luciano
L
Gu
Hua
H
D000818:Animals; D000906:Antibodies / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects / Q000235:genetics; D051017:Apoptosis Regulatory Proteins; D002135:Calcium-Binding Proteins / Q000235:genetics* / Q000378:metabolism; D003907:Dexamethasone / Q000494:pharmacology; D007107:Immune System / Q000254:growth & development; D051379:Mice; D008817:Mice, Mutant Strains; D011948:Receptors, Antigen, T-Cell / Q000276:immunology / Q000378:metabolism; D013601:T-Lymphocytes / Q000187:drug effects / Q000473:pathology / Q000502:physiology*; D019014:fas Receptor / Q000276:immunology / Q000378:metabolism
D000906:Antibodies; D051017:Apoptosis Regulatory Proteins; D002135:Calcium-Binding Proteins; C490815:Pdcd6 protein, mouse; D011948:Receptors, Antigen, T-Cell; D019014:fas Receptor; D003907:Dexamethasone