Reduced global genomic repair of ultraviolet light-induced cyclobutane pyrimidine dimers in simian virus 40-transformed human cells

Molecular Carcinogenesis

Volumn 29, Issue 1, 2000, Pages 17-24

  Inan, Mehmet Sait ^a   Place, Robert ^a   Tolmacheva, Veronica ^a   Wang, Qian Shu ^a   Hubbard, Andrea K ^a   Rosenberg, Daniel W ^a   Giardina, Charles ^a  

^a UNIVERSITY OF CONNECTICUT   (United States)

Author keywords

Large T antigen; Nucleotide excision repair; p53; Simian virus 40; Ultraviolet irradiation

Indexed keywords

CYCLOBUTANE DERIVATIVE; DIHYDROFOLATE REDUCTASE; DOUBLE STRANDED DNA; MESSENGER RNA; MONOCLONAL ANTIBODY; PROTEIN P53; PYRIMIDINE DERIVATIVE; VIRUS LARGE T ANTIGEN;

ARTICLE; EXCISION REPAIR; FIBROBLAST CULTURE; GENOME; HUMAN; HUMAN CELL; NONHUMAN; PRIORITY JOURNAL; SIMIAN VIRUS 40; TUMOR SUPPRESSOR GENE; ULTRAVIOLET IRRADIATION; VIRUS CELL TRANSFORMATION;

CELL LINE, TRANSFORMED; DNA REPAIR; HUMAN; PYRIMIDINE DIMERS; SIMIAN VIRUS 40; SUPPORT, NON-U.S. GOV'T; SUPPORT, U.S. GOV'T, P.H.S.; TETRAHYDROFOLATE DEHYDROGENASE; ULTRAVIOLET RAYS;

EID: 0033779869     PISSN: 08991987     EISSN: None     Source Type: Journal    
DOI: 10.1002/1098-2744(200009)29:1<17::AID-MC3>3.0.CO;2-E     Document Type: Article

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39. Human cells compromised for p53 function exhibit defective global and transcription-coupled nucleotide excision repair, whereas cells compromised for pRb function are defective only in global repair
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