title: CtIP is required for DNA damage-dependent induction of P21.
abstract: DNA endonuclease CtIP is involved in both DNA double-strand break (DSB) repair and transcriptional repression/activation. The cyclin-dependent kinase inhibitor P21, which is induced at transcription level in response to a variety of stresses, controls G₁/S transition. In this report, we found that CtIP bound to the P21 promoter, and this binding was enhanced in response to DNA damage. Concomitantly, ectopic expression of CtIP increased P21 promoter activity, and this increment was enhanced upon camptothecin treatment. Conversely, DNA damage failed to induce P21 gene expression in CtIP-deficient cells. Taken together, our data demonstrate that CtIP is required for DNA damage-induced P21 induction.
authors.affiliation: Beijing Key laboratory of DNA Damage Response; Capital Normal University; College of Life Sciences; Beijing, China.
authors.forename: Bo
authors.initials: B
authors.lastname: Liu
authors.affiliation: Beijing Key laboratory of DNA Damage Response; Capital Normal University; College of Life Sciences; Beijing, China.
authors.forename: Rixin
authors.initials: R
authors.lastname: Cong
authors.affiliation: Beijing Key laboratory of DNA Damage Response; Capital Normal University; College of Life Sciences; Beijing, China.
authors.forename: Bin
authors.initials: B
authors.lastname: Peng
authors.affiliation: Beijing Key laboratory of DNA Damage Response; Capital Normal University; College of Life Sciences; Beijing, China.
authors.forename: Bingtao
authors.initials: B
authors.lastname: Zhu
authors.affiliation: Beijing Key laboratory of DNA Damage Response; Capital Normal University; College of Life Sciences; Beijing, China.
authors.forename: Gelin
authors.initials: G
authors.lastname: Dou
authors.affiliation: Beijing Key laboratory of DNA Damage Response; Capital Normal University; College of Life Sciences; Beijing, China.
authors.forename: Haiyan
authors.initials: H
authors.lastname: Ai
authors.affiliation: College of Life Sciences; Wuhan University; Wuhan, Hubei, China.
authors.forename: Xiaodong
authors.initials: X
authors.lastname: Zhang
authors.affiliation: Department of Genetics and Case Comprehensive Cancer Center; Case Western Reserve University; Cleveland, OH USA.
authors.forename: Zhenghe
authors.initials: Z
authors.lastname: Wang
authors.affiliation: Beijing Key laboratory of DNA Damage Response; Capital Normal University; College of Life Sciences; Beijing, China.
authors.forename: Xingzhi
authors.initials: X
authors.lastname: Xu
mesh_terms: D002352:Carrier Proteins / Q000235:genetics* / Q000378:metabolism; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000235:genetics* / Q000378:metabolism; D004249:DNA Damage / Q000235:genetics*; D004706:Endodeoxyribonucleases; D059585:G1 Phase Cell Cycle Checkpoints / Q000235:genetics*; D018507:Gene Expression Regulation, Developmental; D006801:Humans; D061986:MCF-7 Cells; D009687:Nuclear Proteins / Q000235:genetics* / Q000378:metabolism; D011401:Promoter Regions, Genetic
chemical_list: D002352:Carrier Proteins; D050759:Cyclin-Dependent Kinase Inhibitor p21; D009687:Nuclear Proteins; D004706:Endodeoxyribonucleases; C410741:RBBP8 protein, human
keywords: DNA damage; DNA endonuclease CtIP; P21