Introductory review: involvement of ADP-ribosylation in cellular recovery from some forms of DNA damage.
There is substantial evidence that ADP-ribosylation is stimulated in response to DNA strand breaks produced directly by a damaging agent or during excision repair processes. The report of a reduced stimulation of ADPRT activity in irradiated ataxia telangiectasia cells has recently stimulated a wide interest in the role of ADP-ribosylation in cellular radiation response. The resulting studies, some of which are presented at this conference, demonstrate that cellular recovery from radiation damage can be significantly impaired if ADP-ribosylation is inhibited to a sufficiently low level. The implication is that the repair of DNA lesions is affected. This review summarizes the involvement of the enzyme ADPRT and the extent of ADP-ribosylation in the repair of DNA damage and of cellular recovery.
D000246:Adenosine Diphosphate Ribose / Q000378:metabolism*; D000818:Animals; D001260:Ataxia Telangiectasia / Q000201:enzymology / Q000235:genetics; D002467:Cell Nucleus / Q000201:enzymology; D002470:Cell Survival / Q000187:drug effects / Q000528:radiation effects; D002478:Cells, Cultured; D002843:Chromatin; D002869:Chromosome Aberrations; D004247:DNA / Q000528:radiation effects; D004260:DNA Repair / Q000187:drug effects; D004261:DNA Replication; D006801:Humans; D009702:Nucleoside Diphosphate Sugars / Q000378:metabolism*; D009713:Nucleotidyltransferases / Q000037:antagonists & inhibitors / Q000378:metabolism; D011065:Poly(ADP-ribose) Polymerases; D051381:Rats; D012854:Sister Chromatid Exchange / Q000528:radiation effects
D002843:Chromatin; D009702:Nucleoside Diphosphate Sugars; D000246:Adenosine Diphosphate Ribose; D004247:DNA; D011065:Poly(ADP-ribose) Polymerases; D009713:Nucleotidyltransferases