TFIIH functions are altered by the P210BCR-ABL oncoprotein produced on the Philadelphia chromosome

Yoshiro Maru , Etienne Bergmann , Frédéric Coin (1, 2) , Jean-Marc Egly (1, 2) , Masabumi Shibuya

1 IGBMC - Institut de génétique et biologie moléculaire et cellulaire
2 IGBMC - Institut de Génétique et de Biologie Moléculaire et Cellulaire

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.

Domaines: Biochimie, Biologie Moléculaire

Yoshiro Maru, Etienne Bergmann, Frédéric Coin, Jean-Marc Egly, Masabumi Shibuya. TFIIH functions are altered by the P210BCR-ABL oncoprotein produced on the Philadelphia chromosome. Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis, 2001, 483 (1-2), pp.83-88. ⟨10.1016/s0027-5107(01)00229-9⟩. ⟨hal-04121555⟩