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Biomedical and Environmental Sciences ; (12): 80-84, 2016.
Article Dans Anglais | WPRIM | ID: wpr-258850

Résumé

The molecular mechanism of DNA damage induced by hydroquinone (HQ) remains unclear. Poly(ADP-ribose) polymerase-1 (PARP-1) usually works as a DNA damage sensor, and hence, it is possible that PARP-1 is involved in the DNA damage response induced by HQ. In TK6 cells treated with HQ, PARP activity as well as the expression of apoptosis antagonizing transcription factor (AATF), PARP-1, and phosphorylated H2AX (γ-H2AX) were maximum at 0.5 h, 6 h, 3 h, and 3 h, respectively. To explore the detailed mechanisms underlying the prompt DNA repair reaction, the above indicators were investigated in PARP-1-silenced cells. PARP activity and expression of AATF and PARP-1 decreased to 36%, 32%, and 33%, respectively, in the cells; however, γ-H2AX expression increased to 265%. Co-immunoprecipitation (co-IP) assays were employed to determine whether PARP-1 and AATF formed protein complexes. The interaction between these proteins together with the results from IP assays and confocal microscopy indicated that poly(ADP-ribosyl)ation (PARylation) regulated AATF expression. In conclusion, PARP-1 was involved in the DNA damage repair induced by HQ via increasing the accumulation of AATF through PARylation.


Sujets)
Humains , Antioxydants , Toxicité , Protéines régulatrices de l'apoptose , Génétique , Métabolisme , Lignée cellulaire , Altération de l'ADN , Régulation de l'expression des gènes , Extinction de l'expression des gènes , Histone , Génétique , Métabolisme , Hydroquinones , Toxicité , Poly (ADP-Ribose) polymerase-1 , Poly(ADP-ribose) polymerases , Génétique , Métabolisme , Transport des protéines , Protéines de répression , Génétique , Métabolisme
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