## Abstract The p53 tumor suppressor protein is a critical mediator of cell cycle arrest and apoptosis in response to genotoxic stress. Abrogation of p53 function is a major feature of tumor development and may result in a compromised DNA‐damage response. In our study, we examined the effect of exp
ZNF143 activates gene expression in response to DNA damage and binds to cisplatin-modified DNA
✍ Scribed by Hiroshi Ishiguchi; Hiroto Izumi; Takayuki Torigoe; Yoichiro Yoshida; Hiroshi Kubota; Sadatoshi Tsuji; Kimitoshi Kohno
- Publisher
- John Wiley and Sons
- Year
- 2004
- Tongue
- French
- Weight
- 743 KB
- Volume
- 111
- Category
- Article
- ISSN
- 0020-7136
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✦ Synopsis
Abstract
We have identified a cisplatin‐inducible gene, the mitochondrial ribosomal protein S11 (MRP S11) gene, by means of mRNA differential display. Functional analysis of the MRP S11 promoter showed that a Staf binding site in the promoter is required for both basal promoter activity and cisplatin‐inducible activity. We also found that Staf binding activity is significantly increased in nuclear extracts from cells treated with cisplatin. ZNF 143 and ZNF 76 are human homologues of the Xenopus transcriptional activator, Staf. ZNF 143 expression is induced by cisplatin but ZNF 76 expression is not. However, ZNF 143 expression is not induced by transplatin, which is clinically ineffective. ZNF143 is an inducible gene by other DNA damaging agents such as γ‐irradiation, etoposide and adriamycin. ZNF 143 also binds preferentially to cisplatin‐modified DNA. These results suggest that ZNF 143 participates in cellular responses to DNA damage. © 2004 Wiley‐Liss, Inc.
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