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Death genes

Arch, R. H., R. W. Gedrich, and C. B. Thompson, Tumor necrosis factor receptor-associated factors (TRAFs) — a family of adapter proteins that regulates life and death. Genes Dev, 1998, 12(18), 2821-30. [Pg.91]

Yl. Yuan, J., Shaham, S., Ledoux, S., Ellis, H. M., and Horvitz, H. R., The C. elegans cell death gene ced-3 encodes a protein similar to mammaUan interleukin-1 beta-converting enzyme. Cell 75, 641-652(1993). [Pg.107]

Mean survival time of 1372 days 50% dead in 1457 days 50% dead in 1224 days 50% dead in 978 days anemia 50% dead in 653 days anemia 50% dead in 187 days anemia Leucocyte reduction in 6 days blood chemistry normal after 90 days Increased frequency of sister chromatid exchange at 0.005 Gy increased numbers of chromosomal aberrations at >0.02 Gy no significant increase in cell death Genes modifying cytoskeletal development adversely affected at all doses within 3 h by both high LET (neutrons) and low LET (gamma rays. X-rays) radiations... [Pg.1764]

Was this youT answer Leonard Hayflickofthe University of California at San Francisco, says people are like cars because they age reliably even though there s nothing in the blueprints that shows a process for doing it. In other words, there is no death gene, no mechanism that kills us off after a... [Pg.73]

Perrin FE, Boisset G, Docquier M, Schaad O, Descombes P, Kato AC. No widespread induction of cell death genes occurs in pure motoneurons in an amyotrophic lateral sclerosis mouse model. Hum Mol Genet 2005 14(21) 3309-3320. [Pg.289]

Bim/BOD (Bcl-2 interacting mediator of cell death/Bcl-2 related ovarian death gene) 1 Engidawork et al. 2001b... [Pg.286]

Growth factors 4 Sunival genes 4 Death genes f Overactivation of tumor Suppressor genes... [Pg.69]

Figure 21. Schematic of activation of the NF-xB transcription factor. Phosphorylation of the inhibitor protein IkB results in release of the sequestered NF-xB to the cytosol. NF-xB then translocates into the nucleus followed by phosphorylation and binds to the promoter region of the target gene. NF-xB transcription factor can regulate the transcription of either survival or pro-death genes See text for more detailed explanation. Figure 21. Schematic of activation of the NF-xB transcription factor. Phosphorylation of the inhibitor protein IkB results in release of the sequestered NF-xB to the cytosol. NF-xB then translocates into the nucleus followed by phosphorylation and binds to the promoter region of the target gene. NF-xB transcription factor can regulate the transcription of either survival or pro-death genes See text for more detailed explanation.
N. Maulik, R. M. Engelman, J. A. Rousou, J.E. Flack 3rd, D. Deaton, D.K. Das, Ischemic preconditioning reduces apoptosis by upregulating anti-death gene bcl-2, Circulation 100, Suppl 11-369-375 (1999). [Pg.193]

Zong, W.X., Ditsworth, D., Bauer, D.E., Wang, Z.Q., and Thompson, C.B. (2004). Alkylating DNA damage stimulates a regulated form of necrotic cell death. Genes Dev 18, 1272-82. [Pg.292]

Mach JM, Castillo AR, Hoogstraten R, Greenberg JT (2001) The Arabidopsis Accelerated Cell Death Gene ACD2 Encodes Red Chlorophyll Catabolite Reductase and Suppresses the Spread of Disease Symptoms. Proc Natl Acad Sci USA 98 771... [Pg.41]

Figure 18.2 Phylogenetic analysis segregates the human caspases into two major subfamilies, one based on caspase-1 previously referred to as ICE, for interleukin-converting enzyme, and the other based on similarities to the C. elegans cell death gene, ced-3. Further classification of the caspases is possible into those that mediate cytokine maturation that are involved in inflammation, those with a short prodomain involved in the effector phase of apoptosis (shown boxed), and those with a long prodomain that are involved in the initiator phase of apoptosis (not boxed). Note evolutionary distances are not accurately represented in this dendrogram. (Adapted from Nicholson, D.W. (1999). Caspase structure, proteolytic substrates, and function during apoptotic cell death. Cell Death Differ 6 1028-1042.)... Figure 18.2 Phylogenetic analysis segregates the human caspases into two major subfamilies, one based on caspase-1 previously referred to as ICE, for interleukin-converting enzyme, and the other based on similarities to the C. elegans cell death gene, ced-3. Further classification of the caspases is possible into those that mediate cytokine maturation that are involved in inflammation, those with a short prodomain involved in the effector phase of apoptosis (shown boxed), and those with a long prodomain that are involved in the initiator phase of apoptosis (not boxed). Note evolutionary distances are not accurately represented in this dendrogram. (Adapted from Nicholson, D.W. (1999). Caspase structure, proteolytic substrates, and function during apoptotic cell death. Cell Death Differ 6 1028-1042.)...
Kumar, S., Kinoshita, M., Noda, M., Copeland, N.G. and Jenkins, N.A. (1994) Induction of apoptosis by the mouse Nedd2 gene, which encodes a protein similar to the product of the Caenorhabditis elegans cell death gene ced-3 and the... [Pg.116]

Induction of apoptosis in fibroblasts by IL-1 betaconverting enzyme, a mammalian homolog of the C. ele-gans cell death gene ced-. Cell 75 653-660. [Pg.117]


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See also in sourсe #XX -- [ Pg.18 ]




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