Poly(ADP-ribosyl)ation of Apoptosis Antagonizing Transcription Factor Involved in Hydroquinone-Induced DNA Damage Response.
- Author:
Xiao Xuan LING
1
;
Jia Xian LIU
2
;
Lin YUN
2
;
Yu Jun DU
3
;
Shao Qian CHEN
4
;
Jia Long CHEN
5
;
Huan Wen TANG
2
;
Lin Hua LIU
2
Author Information
- Publication Type:Letter
- MeSH: Antioxidants; toxicity; Apoptosis Regulatory Proteins; genetics; metabolism; Cell Line; DNA Damage; drug effects; Gene Expression Regulation; drug effects; Gene Silencing; Histones; genetics; metabolism; Humans; Hydroquinones; toxicity; Poly (ADP-Ribose) Polymerase-1; Poly(ADP-ribose) Polymerases; genetics; metabolism; Protein Transport; Repressor Proteins; genetics; metabolism
- From: Biomedical and Environmental Sciences 2016;29(1):80-84
- CountryChina
- Language:English
- Abstract: 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.
