Get Apoptosis Genes PDF

By J. W. Wilson, C. Booth, C. S. Potten (auth.), James W. Wilson, Catherine Booth, Christopher S. Potten (eds.)

Apoptosis, or programmed telephone loss of life, is a average method through which broken or undesirable cells are dismantled in an orderly and atraumatic model. it really is of serious value in improvement, homeostasis, and cellphone inhabitants regulate. study during the last decade is now permitting scientists to appreciate how genes and the protein items engage to manage apoptosis. This has resulted in the present place the place researchers are able to without delay adjust the motion of key proteins via gene treatment and antisense oligonucleotides.
Apoptosis Genes provides a present evaluate of key genes excited about the regulate of apoptosis learn including ideas on destiny customers and scientific functions. whereas there are numerous books written on apoptosis, Apoptosis Genes bargains in particular with the law of apoptosis. Given the elevated curiosity within the position of apoptosis genes in disorder tactics, this paintings could be worthwhile to researchers investigating melanoma, autoimmune illness, viral an infection, heart problems, neurodegenerative issues, AIDS, osteoporosis, and aging.

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Exp. Cell Res. 211: 90·98. , et al. (1996) p53-dependent apoptosis suppresses radiationinduced teratogenesis. Nature. Med. 2: 577-580. Okamoto,K and Beach,D. (1994) Cyclin G is a transcriptional target of the p53 tumor suppressor protein. EMBO J. 13: 4816-4822. , et al. (1992) Amplification of a gene encoding a p53-binding protein in human sarcomas. Nature 358: 80-83. , et al. (1993) Oncoprotein mdm2 conceals the activation domain of tumor suppressor p53. Nature 362: 857-860. Pan,H. E. (1994) Altered cell cycle regulation in the lens of HPV-16 E6 or E7 transgenic mice: implications for tumor suppressor gene function in development.

Et al. (1997) Transgenic mouse model for studying the transcriptional activity of the p53 protein: age- and tissue-dependent changes in radiation-induced activation during embryogenesis. EMBO J. 16: 1381-1390. M. and Oren,M. (1996) p53 in growth control and neoplasia. Biochem. Biophys. Acta 1287: 77-102. , et al. (1994) Hypoxia induces accumulation of p53 protein, but activation of a GI phase checkpoint by low-oxygen conditions is independent of p53 status. Mol. Cell Bioi. 14: 6264-6277. , et al.

A. , e/ al. (1992) Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours. Nalure 356: 215-221. , e/ al. (1993) WAFl, a potential mediator of p53 tumour suppression. Cell 75: 817 -825. W. J. (1989) The p53 proto-oncogene can act as a suppressor of transformation. Cell 57: 1083-1093. , Prives,C and Oren,M. (1996) A mutant p53 that discriminates between p53responsive genes cannot induce apoptosis. Mol. Cell Bio/. 16: 4961-4971. , Haessler,C. and Brandner,G. (1993) Induction of nuclear accumulation of the tumour suppressor protein p53 by DNA damaging agents.

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