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PMID:8640868

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Citation

Tamura, A, Katsumata, M, Greene, MI and Yui, K (1996) Inhibition of apoptosis and augmentation of lymphoproliferation in bcl-2 transgenic Fas/Fas ligand-defective mice. Cell. Immunol. 168:220-8

Abstract

Mice defective in Fas (CD95 or APO-1) or its ligand (lpr or gld mice) develop age-dependent lymphadenopathy and systemic autoimmune disease. T cells accumulating in the lymph nodes of these mice express reduced levels of Bcl-2 protein and are susceptible to spontaneous and glucocorticoid-induced apoptosis. We backcrossed bcl-2 transgenic mice to lpr and gld mice to homozygosity to determine the effects of Bcl-2 overexpression. T cells in these mice were resistant to spontaneous and glucocorticoid-induced apoptosis in vitro. Moreover, the accumulation of CD4(-)CD8(-) T cells in the lymph nodes and the spleens was augmented, suggesting that a Bcl-2-dependent mechanism regulating the number of T cells residing in the peripheral lymphoid organs in addition to the Fas-mediated pathway exists.

Links

PubMed Online version:10.1006/cimm.1996.0069

Keywords

Animals; Antigens, CD95/genetics; Antigens, CD95/physiology; Apoptosis/drug effects; Apoptosis/physiology; Cells, Cultured; Crosses, Genetic; Dexamethasone/pharmacology; Drug Resistance; Fas Ligand Protein; Gene Expression Regulation/drug effects; Humans; Lymph Nodes/cytology; Lymphocyte Activation/physiology; Membrane Glycoproteins/deficiency; Membrane Glycoproteins/genetics; Mice; Mice, Inbred C3H; Mice, Mutant Strains; Mice, Transgenic; Proto-Oncogene Proteins/biosynthesis; Proto-Oncogene Proteins/genetics; Proto-Oncogene Proteins/physiology; Proto-Oncogene Proteins c-bcl-2; Signal Transduction; Species Specificity; Spleen/cytology; T-Lymphocyte Subsets/drug effects; T-Lymphocyte Subsets/physiology; Thymus Gland/cytology; Transgenes

Significance

Annotations

Gene product Qualifier GO ID GO term name Evidence Code with/from Aspect Notes Status


See also

References

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