Radiosensitivity in Nijmegen Breakage Syndrome cells is attributable to a repair defect and not cell cycle che ckpoint defects

Cancer Research

Volumn 60, Issue 17, 2000, Pages 4881-4888

  Girard, P M ^a   Foray, N ^a   Stumm, M ^a   Waugh, A ^a   Riballo, E ^a   Maser, R S ^a   Phillips, W P ^a   Petrini, J ^a   Arlett, C F ^a   Jeggo, P A ^a  

^a UNIVERSITY OF SUSSEX   (United Kingdom)

Author keywords

[No Author keywords available]

Indexed keywords

ARTICLE; CELL CYCLE; CELL CYCLE G2 PHASE; CHROMOSOME BREAKAGE; CHROMOSOME SEGREGATION; DNA DAMAGE; DNA REPAIR; DNA STRAND BREAKAGE; EXCISION REPAIR; HUMAN; HUMAN CELL; IRRADIATION; NIJMEGEN BREAKAGE SYNDROME; PRIORITY JOURNAL; RADIOSENSITIVITY;

ABNORMALITIES, MULTIPLE; ATAXIA TELANGIECTASIA; CELL CYCLE; CELL LINE; CELL SURVIVAL; CHROMOSOME BREAKAGE; CHROMOSOMES, HUMAN; DNA; DNA DAMAGE; DNA REPAIR; FIBROBLASTS; HUMANS; INTERPHASE; MITOSIS; PHOSPHORYLATION; PROTEIN KINASES; PROTEIN-SERINE-THREONINE KINASES; RADIATION TOLERANCE; SYNDROME; TUMOR SUPPRESSOR PROTEIN P53;

EID: 0034282753     PISSN: 00085472     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

References (54)

1. DNA damage triggers a prolonged p53-dependent G1 arrest and long-term induction of Cip1 in normal human fibroblasts
2. Linkage of ATM to cell cycle regulation by the Chk2 protein kinase
3. DNA-dependent protein kinase is not required for the p53-dependent response to DNA damage
4. Leukemia and lymphoma in ataxia telangiectasia
5. The ATM gene and the radiobiology of ataxia-telangiectasia
6. Radiosensitivity in ataxia-telangiectasia: Anomalies in radiation-induced cell cycle delay
7. Radiation-induced G2 delay and spontaneous chromosome aberrations in ataxia-telangiectasia homozygotes and heterozygotes
8. A single ataxia telangiectasia gene with a product similar to PI 3-kinase
9. Splitting the ATM: Distinct repair and checkpoint defects in ataxia-telangiectasia
10. Cellular radiosensitivity in ataxia-telangiectasia
11. Correspondence re: M. Stephen Meyn, Ataxia telangiectasia and cellular responses to DNA damage
12. Ataxia-telangiectasia. Is ATM a sensor of oxidative damage and stress?
13. Hypersensitivity of ataxia-telangiectasia fibroblasts to ionizing radiation is associated with a repair deficiency of DNA double-strand breaks
14. A new chromosomai instability disorder: The Nijmegan breakage syndrome
15. Nijmegen breakage syndrome
16. Ataxia telangiectasia variants (Nijmegen Breakage Syndrome)
17. Characterization of cell cycle checkpoint responses after ionizing radiation in Nijmegen breakage syndrome cells
18. Radiation induction of p53 in cells from Nijmegen breakage syndrome is defective but not similar to ataxia-telangiectasia
19. Nijmegen breakage syndrome cells fail to induce the p53-mediated DNA damage response following exposure to ionizing radiation
20. Impaired p53-mediated DNA damage response, cell-cycle disturbance and chromosome aberrations in Nijmegen breakage syndrome lymphoblastoid cell lines
21. The hMre11/hRad50 protein complex and Nijmegen breakage syndrome: Linkage of double-strand break repair to the cellular DNA damage response
22. Nibrin, a novel DNA double-strand break repair protein, is mutated in Nijmegen breakage syndrome
23. Interaction of Mre11 and Rad50: Two proteins required for DNA repair and meiosis-specific double-strand break formation in Saccharomyces cerevisiae
24. The DNA doublestrand break repair gene hMREII is mutated in individuals with an ataxia-telangiectasia-like disorder
25. Mutations in two Ku homologs define a DNA end-joining repair pathway in Saccharomyces cerevisiae
26. Cell cycle and genetic requirements of two pathways of nonhomologous end-joining repair of double-strand breaks in Saccharomyces cerevisiae
27. Effects of mutations of RAD50, RAD51, RAD52, and related genes on illegitimate recombination in Saccharomyces cerevisiae
28. The Mre11-Rad50-xrs2 protein complex facilitates homologous recombination-based double-strand break repair in Saccharomyces cerevisiae
29. The many interfaces of Mre11
30. Comparative human cellular radiosensitivity. I. The effect of SV40 immortalisation on the gamma-irradiation survival of skin derived fibroblasts from normal individuals and from ataxia-telangiectasia patients and heterozygotes
31. In vivo competition between a metallothionein regulatory element and the SV40 enhancer
32. A DNA double-strand break defective fibroblast cell line, (180BR), derived from a radiosensitive patient represents a new mutant phenotype
33. Human tumour cell kinetics using a monoclonal antibody against iododeoxyuridine: Intratumour sampling variations
34. Dose-rate effect on radiation-induced DNA double-strand breaks in the human fibroblast HF19 cell line
35. Induction and rejoining of DNA double strand breaks and interphase chromosome breaks after exposure to X-rays in one normal and two hypersensitive human fibroblast cell lines
36. X-ray-induced breakage and rejoining of human interphase chromosomes
37. DNA breakage and repair
38. On the nature of a defect in cells from individuals with ataxia-telangiectasia
39. Radiation-induced micronuclei in human fibroblasts in relation to clonogenic radiosensitivity
40. Radiosensitivity in ataxia-telangiectasia: A new explanation
41. Effect of ionising radiation on DNA synthesis in ataxia-telangiectasia cells
42. A mammalian cell cycle checkpoint pathway utilizing p53 and GADD45 is defective in ataxia-telangiectasia
43. Defects in the kinetics of repair of DNA double-strand breaks and inhibition of DNA-synthesis in the ataxia-telangiectasia AT5BI-VA cell-line-comparison to a corrected hybrid, ATXBC
44. Combined immunodeficiency associated with increased apoptosis of lymphocytes and radiosensitivity of fibroblasts
45. Immortalization and characterization of Nijmegen Breakage syndrome fibroblasts
46. Further delineation of the Nijmegan breakage syndrome
47. Mutations associated with variant phenotypes in ataxia telangiectasia
48. Marked elevation of intrachromosomal mitotic recombination: A new facet of the ataxia telangiectasia phenotype
49. XRCC3 promotes homology-directed repair of DNA damage in mammalian cells
50. A new chromosomal instability disorder confirmed by complementation studies
51. hMre11 and hRad50 nuclear foci are induced during the normal cellular response to DNA double-strand breaks