TFIIH functions are altered by the P210BCR-ABL oncoprotein produced on the Philadelphia chromosome.
P210BCR-ABL counteracted against the complementary effect of XPB on DNA repair when ultraviolet (UV)-sensitive 27-1 cells were treated with UV or cisplatin but not with hydrogen peroxide. Wortmannin, an inhibitor of PI3 kinase did not affect its anti-repair effect. Enhanced recruitment of p44 with TFIIH after cisplatin treatment is inhibited by the expression of P210BCR-ABL in a kinase activity-dependent manner. Although purified TFIIH from P210BCR-ABL expressor and non-expressor showed almost no difference in molar ratio of each component, the in vitro activity of TFIIH was decreased by 5-10% in repair assay but was increased by more than two-fold in transcription assay.
Maru
Y
Y
Department of Genetics, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, 108-0071, Tokyo, Japan. ymaru@ims.u-tokyo.ac.jp
Bergmann
E
E
Coin
F
F
Egly
J M
JM
Shibuya
M
M
D000818:Animals; D016466:CHO Cells; D002945:Cisplatin / Q000633:toxicity; D006224:Cricetinae; D004265:DNA Helicases; D004260:DNA Repair; D004268:DNA-Binding Proteins / Q000235:genetics / Q000378:metabolism; D016044:Fusion Proteins, bcr-abl / Q000235:genetics* / Q000378:metabolism*; D006801:Humans; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000235:genetics / Q000378:metabolism; D010677:Philadelphia Chromosome; D051758:Transcription Factor TFIIH; D014157:Transcription Factors / Q000235:genetics* / Q000378:metabolism*; D019473:Transcription Factors, TFII; D014162:Transfection
D004268:DNA-Binding Proteins; D014157:Transcription Factors; D019473:Transcription Factors, TFII; C072022:XPBC-ERCC-3 protein; D051758:Transcription Factor TFIIH; D016044:Fusion Proteins, bcr-abl; D004265:DNA Helicases; D002945:Cisplatin