Li-Fraumeni syndrome fibroblasts homozygous for p53 mutations are deficient in global DNA repair but exhibit normal transcription-coupled repair and enhanced UV resistance

Proceedings of the National Academy of Sciences of the United States of America

Volumn 92, Issue 19, 1995, Pages 8876-8880

  Ford, James M ^a   Hanawalt, Philip C ^a  

^a STANFORD UNIVERSITY   (United States)

Author keywords

apoptosis; cyclobutane pyrimidine dimer; DNA damage; p53 tumor suppressor gene; TP53

Indexed keywords

CYCLOBUTANE; PROTEIN P53; PYRIMIDINE DIMER;

APOPTOSIS; ARTICLE; CYTOTOXICITY; DNA DAMAGE; DNA REPAIR; FAMILIAL CANCER; GENE MUTATION; HUMAN; HUMAN CELL; PRIORITY JOURNAL; SKIN FIBROBLAST; TUMOR SUPPRESSOR GENE; ULTRAVIOLET RADIATION;

APOPTOSIS; CELL SURVIVAL; CLONE CELLS; COMPARATIVE STUDY; DNA REPAIR; DOSE-RESPONSE RELATIONSHIP, RADIATION; FIBROBLASTS; HOMOZYGOTE; HUMAN; LI-FRAUMENI SYNDROME; MICROSCOPY, FLUORESCENCE; MUTATION; NEOPLASMS; PROTEIN P53; PYRIMIDINE DIMERS; RADIATION TOLERANCE; SUPPORT, NON-U.S. GOV'T; SUPPORT, U.S. GOV'T, P.H.S.; TETRAHYDROFOLATE DEHYDROGENASE; TRANSCRIPTION, GENETIC; ULTRAVIOLET RAYS;

EID: 0029029741     PISSN: 00278424     EISSN: None     Source Type: Journal    
DOI: 10.1073/pnas.92.19.8876     Document Type: Article

References (30)