Xeroderma pigmentosum p48 gene enhances global genomic repair and suppresses UV-induced mutagenesis

Molecular Cell

Volumn 5, Issue 4, 2000, Pages 737-744

  Tang, Jean Y ^a,b   Hwang, Byung Joon ^a,b   Ford, James M ^a,b   Hanawalt, Philip C ^b   Chu, Gilbert ^a,b  

^a STANFORD UNIVERSITY SCHOOL OF MEDICINE   (United States)

^b STANFORD UNIVERSITY   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CYCLOBUTANE DERIVATIVE; DNA; PYRIMIDINE DIMER;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CANCER SUSCEPTIBILITY; CELL LINE; DNA BINDING; DNA REPAIR; GENE EXPRESSION; GENE MUTATION; GENETIC TRANSCRIPTION; GENETIC TRANSFECTION; HAMSTER; HUMAN; HUMAN CELL; MOUSE; NONHUMAN; RADIATION MUTAGENESIS; RODENT; ULTRAVIOLET IRRADIATION; XERODERMA PIGMENTOSUM;

ANIMALIA; CRICETINAE; RODENTIA;

EID: 0033636515     PISSN: 10972765     EISSN: None     Source Type: Journal    
DOI: 10.1016/S1097-2765(00)80252-X     Document Type: Article

References (41)

1. Mammalian DNA nucleotide excision repair reconstituted with purified protein components
2. Expression of a mammalian DNA photolyase confers light-dependent repair activity and reduces mutations of UV-irradiated shuttle vectors in xeroderma pigmentosum cells
3. DNA repair in an active gene: Removal of pyrimidine dimers from the DHFR gene of CHO cells is much more efficient than in the genome overall
4. Nucleotide excision repair syndromes: Xeroderma pigmentosum, Cockayne syndrome, and trichothiodystrophy
5. Xeroderma pigmentosum group E cells lack a nuclear factor that binds to damaged DNA
6. Chromosomal localization and cDNA cloning of the genes (DDB1 and DDB2) for the p127 and p48 subunits of a human damage-specific DNA binding protein
7. The role of UV-B light in skin carcinogenesis through the analysis of p53 mutations in squamous cell carcinomas of hairless mice
8. Expression of wild-type p53 is required for efficient global genomic nucleotide excision repair in UV-irradiated human fibroblasts
9. p53 mutations in skin and internal tumors of xeroderma pigmentosum patients belonging to the complementation group C
10. Transcription-coupled repair and human disease
11. Purification and characterization of a protein that binds to damaged DNA
12. Isolation of a cDNA encoding a UV-damaged DNA binding factor defective in xeroderma pigmentosum group E cells
13. p48 activates a UV-damaged DNA binding factor and is defective in xeroderma pigmentosum group E cells that lack the binding activity
14. Expression of the p48 xeroderma pigmentosum gene is p53-dependent and is involved in global genomic repair
15. A newly identified patient with clinical xeroderma pigmentosum phenotype has a non-sense mutation in the DDB2 gene and incomplete repair in (6-4) photoproducts
16. hRAD30 mutations in the variant form of xeroderma pigmentosum
17. Preferential binding of the xeroderma pigmentosum group A complementing protein to damaged DNA
18. Functional complementation of xeroderma pigmentosum complementation group E by replication protein A in an in vitro system
19. Biochemical heterogeneity in xeroderma pigmentosum complementation group E
20. Altered UV resistance and UV mutational spectrum in repair-proficient murine fibroblasts expressing endonuclease V
21. The XPV (xeroderma pigmentosum variant) gene encodes human DNA polymerase η
22. Selective removal of transcription-blocking DNA damage from the transcribed strand of the mammalian DHFR gene
23. Simultaneous establishment of monoclonal antibodies specific for either cyclobutane pyrimidine dimer or (6-4) photoproduct from the same mouse immunized with ultraviolet-irradiated DNA
24. Cockayne syndrome: Review of 140 cases
25. Erythema, skin cancer risk, and sunscreens
26. Mutations specific to the xeroderma pigmentosum group E Ddb- phenotype
27. Relationship of the xeroderma pigmentosum group E DNA repair defect to the chromatin and DNA binding proteins UV-DDB and replication protein A
28. Xeroderma pigmentosum group E binding factor recognizes a broad spectrum of DNA damage
29. Comparative analysis of binding of human damaged DNA-binding protein (XPE) and Escherichia coli damage recognition protein (uvrA) to the major ultraviolet photoproducts: T[c,s]T, T[t,s]T, T[6-4]T, and T[Dewar]T
30. Xeroderma pigmentosum group C protein complex is the initiator of global genome nucleotide excision repair
31. A 127 kDa component of a UV-damaged DNA-binding complex, which is defective in some xeroderma pigmentosum group E patients, is homologous to a slime mold protein
32. An ultraviolet light-damaged DNA recognition protein absent in xeroderma pigmentosum group E cells binds selectively to pyrimidine (6-4) pyrimidone photoproducts
33. Defective transcription-coupled repair in Cockayne syndrome B mice is associated with skin cancer predisposition
34. Transcription-coupled repair removes both cyclobutane pyrimidine dimers and 6-4 photoproducts with equal efficiency and in a sequential way from transcribed DNA in xeroderma pigmentosum group C fibroblasts
35. Xeroderma pigmentosum complementation group C cells remove pyrimidine dimers selectively from the transcribed strand of active genes
36. Enhanced UV-induced mutagenesis in the UV61 cell line, the Chinese hamster homologue of Cockayne's syndrome B, is associated with defective transcription coupled repair of cyclobutane pyrimidine dimers
37. Order of assembly of human DNA repair excision nuclease
38. DNA damage recognition during nucleotide excision repair in mammalian cells
39. Phenotypic heterogeneity within the first complementation group of UV-sensitive mutants of Chinese hamster cell lines
40. (6-4) photoproducts and not cyclobutane pyrimidine dimers are the main UV-induced mutagenic lesions in Chinese hamster cells