The tumor suppressor p53 can both stimulate and inhibit ultraviolet light-induced apoptosis

Molecular Biology of the Cell

Volumn 11, Issue 8, 2000, Pages 2543-2551

  McKay, B C ^a   Chen, F ^a   Perumalswami, C R ^a   Zhang, F ^a   Ljungman, M ^a  

^a UNIVERSITY OF MICHIGAN COMPREHENSIVE CANCER CENTER   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

PROTEIN P53;

APOPTOSIS; ARTICLE; CELL PROTECTION; HUMAN; HUMAN CELL; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN SYNTHESIS; SIGNAL TRANSDUCTION; TRANSCRIPTION REGULATION; TRANSLATION REGULATION; TUMOR SUPPRESSOR GENE; ULTRAVIOLET RADIATION;

EID: 0033836606     PISSN: 10591524     EISSN: None     Source Type: Journal    
DOI: 10.1091/mbc.11.8.2543     Document Type: Article

References (55)

1. Ultraviolet light induces apoptosis via direct activation of CD95 (fas/APO-1) independently of its ligand CD95L
2. p53 is a rate-limiting factor in the repair of higher-order DNA structure
3. Aberrant p21(WAF1)-dependent growth arrest as the possible mechanism of abnormal resistance to ultraviolet light cytotoxicity in Li-Fraumeni syndrome fibroblast strains heterozygous for TP53 mutations
4. p21-induced cycle arrest in G1 protects cells from apoptosis induced by UV-irradiation or RNA polymerase II blockage
5. Requirement for p53 and p21 to sustain G2 arrest after DNA damage
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7. Dose-dependent effects of DNA-damaging agents on p53-mediated cell cycle arrest
8. p53 levels, functional domains, and DNA damage determine the extent of the apoptotic response of tumor cells
9. Butyrate attenuates BCLXL expression in human fibroblasts and acts in synergy with ionizing radiation to induce apoptosis
10. Transcript cleavage by RNA polymerase II arrested by a cyclobutane pyrimidine dimer in the DNA template
11. Prolonged p53 protein accumulation in trichothiodystrophy fibroblasts dependent on unrepaired pyrimidine dimers on the transcribed strands of cellular genes
12. Wild-type p53 activates transcription in vitro
13. Li-Fraumeni syndrome fibroblasts homozygous for p53 mutations are deficient in global DNA repair but exhibit normal transcription-coupled repair and enhanced UV resistance
14. Expression of wild-type p53 is required for efficient global genomic nucleotide excision repair in UV-irradiated human fibroblasts
15. Protein synthesis required to anchor a mutant p53 protein which is temperature-sensitive for nuclear transport
16. Induction of growth arrest by a temperature-sensitive p53 mutant is correlated with increased nuclear localization and decreased stability of the protein
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29. Differential induction of transcriptionally active p53 following UV or ionizing radiation: Defects in chromosome instability syndromes?
30. Cellular localization and cell cycle regulation by a temperature-sensitive p53 protein
31. Role for p53 in the recovery of transcription and protection against apoptosis induced by ultraviolet light
32. Wildtype p53 is required for heat shock and ultraviolet light enhanced repair of a UV-damaged reporter gene
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35. Expression of wild-type p53 stimulates an increase in both Bax and Bcl-x(L) protein content in HT29 cells
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39. Genetic determinants of p53-induced apoptosis and growth arrest
40. One pyrimidine dimer inactivates expression of a transfected gene in xeroderma pigmentosum cells
41. Ultraviolet radiation-induced apoptosis is mediated by activation of CD-95 (Fas/APO-1)
42. Impaired nucleotide excision repair in UV-irradiated human oral keratinocytes immortalized with type 16 human papillomavirus genome
43. Gene and transcription mapping by radiation effects
44. Ultraviolet-irradiation-induced apoptosis is mediated via ligand independent activation of tumor necrosis factor receptor 1
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49. 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
50. Myc-mediated apoptosis requires wild-type p53 in a manner independent of cell cycle arrest and the ability of p53 to induce p21(waf1/cip1)
51. Ultraviolet radiation down-regulates expression of the cell-cycle inhibitor p21WAF1/CIP1 in human cancer cells independently of p53
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55. Wild-type p53 mediates positive regulation of gene expression through a specific DNA sequence element