Defects in regulation of apoptosis in caspase-2-deficient mice
| Autor: | Keith E. Latham, Arnold H. Greenberg, Andrea Jurisicova, Louise Bergeron, Lianfa Shi, Junying Yuan, Jodi A. Flaws, Sue Varmuza, Gloria I. Perez, En Li, Glen C. Macdonald, Jonathan L. Tilly, Yi Sun, Jessica C.M. Salter, Michael A. Moskowitz, Hideaki Hara |
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| Rok vydání: | 1998 |
| Předmět: |
Male
Programmed cell death Caspase 2 Apoptosis Granzymes Brain Ischemia Mice Genetics Animals fas Receptor Caspase DNA Primers Mice Knockout Motor Neurons B-Lymphocytes biology Base Sequence Amyotrophic Lateral Sclerosis Serine Endopeptidases Proteins Molecular biology Cell biology Granzyme B Mice Inbred C57BL Perforin Granzyme Mice Inbred DBA Brain Injuries Caspases Mutation Nerve Degeneration biology.protein Oocytes Female Intracellular Developmental Biology Research Paper |
| Zdroj: | Genesdevelopment. 12(9) |
| ISSN: | 0890-9369 |
| Popis: | During embryonic development, a large number of cells die naturally to shape the new organism. Members of the caspase family of proteases are essential intracellular death effectors. Herein, we generated caspase-2-deficient mice to evaluate the requirement for this enzyme in various paradigms of apoptosis. Excess numbers of germ cells were endowed in ovaries of mutant mice and the oocytes were found to be resistant to cell death following exposure to chemotherapeutic drugs. Apoptosis mediated by granzyme B and perforin was defective in caspase-2-deficient B lymphoblasts. In contrast, cell death of motor neurons during development was accelerated in caspase-2-deficient mice. In addition, caspase-2-deficient sympathetic neurons underwent apoptosis more effectively than wild-type neurons when deprived of NGF. Thus, caspase-2 acts both as a positive and negative cell death effector, depending upon cell lineage and stage of development. |
| Databáze: | OpenAIRE |
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