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  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-09-12
    Description: Bcl-2 and related cytoplasmic proteins are key regulators of apoptosis, the cell suicide program critical for development, tissue homeostasis, and protection against pathogens. Those most similar to Bcl-2 promote cell survival by inhibiting adapters needed for activation of the proteases (caspases) that dismantle the cell. More distant relatives instead promote apoptosis, apparently through mechanisms that include displacing the adapters from the pro-survival proteins. Thus, for many but not all apoptotic signals, the balance between these competing activities determines cell fate. Bcl-2 family members are essential for maintenance of major organ systems, and mutations affecting them are implicated in cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Adams, J M -- Cory, S -- CA43540/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Aug 28;281(5381):1322-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Institute of Medical Research, Post Office Royal Melbourne Hospital, Victoria 3050, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9735050" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Cell Cycle ; *Cell Survival ; Cysteine Endopeptidases/metabolism ; Cytokines/physiology ; Genes, bcl-2 ; Humans ; Neoplasms/etiology/pathology/therapy ; Organelles/physiology ; Proto-Oncogene Proteins c-bcl-2/chemistry/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1991-11-22
    Description: Numerous cancer-prone strains of mice have been created by the introduction of candidate tumor-promoting genes into fertilized eggs. Each transgenic strain is predisposed to develop specific types of tumors, but they usually arise stochastically because of the need for spontaneous mutation of genes that collaborate with the introduced oncogene. These mice are providing insights into the effects of individual oncogenes on cellular proliferation, differentiation, and viability, as well as on oncogene cooperativity. Their predisposed state imposes sensitivity to viral and chemical carcinogenesis, and the mice should prove valuable in tests of potential carcinogens, therapies, and preventive measures.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Adams, J M -- Cory, S -- CA12421/CA/NCI NIH HHS/ -- CA43540/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 Nov 22;254(5035):1161-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, Melbourne, Victoria, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1957168" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Animals, Genetically Modified ; Genes, Tumor Suppressor ; Leukemia, Experimental/genetics ; Liver Neoplasms/genetics ; Mammary Neoplasms, Experimental/genetics ; Neoplasms, Experimental/*genetics ; Oncogenes ; Pancreatic Neoplasms/genetics ; Precancerous Conditions/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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