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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
MeSH Review

DNA Fragmentation

 
 
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Disease relevance of DNA Fragmentation

 

High impact information on DNA Fragmentation

 

Chemical compound and disease context of DNA Fragmentation

 

Biological context of DNA Fragmentation

 

Anatomical context of DNA Fragmentation

 

Associations of DNA Fragmentation with chemical compounds

  • Both the Ca2+ increase and DNA fragmentation were prevented in cells treated with the inhibitor of protein synthesis, cycloheximide, and DNA fragmentation and cell killing were not detected when cells were incubated in a "Ca2+-free" medium or pretreated with high concentrations of the calcium probe, quin-2 tetraacetoxymethyl ester [26].
  • The effects of C2-ceramide on DNA fragmentation were prevented by the protein kinase C activator phorbol 12-myristate 13-acetate, which suggests the existence of two opposing intracellular pathways in the regulation of apoptosis [27].
  • Induction of DNA fragmentation required the cytoplasmic domain of the mutants and appeared to be mediated by heterotrimeric guanosine triphosphate-binding proteins (G proteins) [28].
  • Inhibition of DNA fragmentation required substantially higher levels of caspase-3 attenuation than that required for blockade of other apoptotic events such as spectrin proteolysis and phosphatidylserine externalization [29].
  • Biochemical pathways of apoptosis: nicotinamide adenine dinucleotide-deficient cells are resistant to tumor necrosis factor or ultraviolet light activation of the 24-kD apoptotic protease and DNA fragmentation [23].
 

Gene context of DNA Fragmentation

 

Analytical, diagnostic and therapeutic context of DNA Fragmentation

References

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  22. Reduction in mitochondrial potential constitutes an early irreversible step of programmed lymphocyte death in vivo. Zamzami, N., Marchetti, P., Castedo, M., Zanin, C., Vayssière, J.L., Petit, P.X., Kroemer, G. J. Exp. Med. (1995) [Pubmed]
  23. Biochemical pathways of apoptosis: nicotinamide adenine dinucleotide-deficient cells are resistant to tumor necrosis factor or ultraviolet light activation of the 24-kD apoptotic protease and DNA fragmentation. Wright, S.C., Wei, Q.S., Kinder, D.H., Larrick, J.W. J. Exp. Med. (1996) [Pubmed]
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