ArticleCell cycle (Georgetown, Tex.)2013
Zinc finger protein 668 interacts with Tip60 to promote H2AX acetylation after DNA damage.
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- ZNF432 stimulates PARylation and inhibits DNA resection to balance PARPi sensitivity and resistance.Nucleic acids research · 2023Article
- Relationship between the Reduced Expression of Zinc Finger Protein 668 in Bladder Cancer and Its Invasiveness.International journal of molecular sciences · 2023Article
- Article
- Post-Translational Modifications by Lipid Metabolites during the DNA Damage Response and Their Role in Cancer.Biomolecules · 2022Review
- ZNF668 deficiency causes a recognizable disorder of DNA damage repair.Human genetics · 2021Article
- Delineating the HMGB1 and HMGB2 interactome in prostate and ovary epithelial cells and its relationship with cancer.Oncotarget · 2018Article
- Caught with One's Zinc Fingers in the Genome Integrity Cookie Jar.Trends in genetics : TIG · 2018Review
- Zinc finger protein 668 suppresses non-small cell lung cancer invasion and migration by downregulating Snail and upregulating E-cadherin and zonula occludens-1.Oncology letters · 2018Article
- Zinc finger proteins in cancer progression.Journal of biomedical science · 2016Review
- Coordinated Regulation of TIP60 and Poly(ADP-Ribose) Polymerase 1 in Damaged-Chromatin Dynamics.Molecular and cellular biology · 2016Article
- TIE2-mediated tyrosine phosphorylation of H4 regulates DNA damage response by recruiting ABL1.Science advances · 2016Article
- mTOR Inhibitors Suppress Homologous Recombination Repair and Synergize with PARP Inhibitors via Regulating SUV39H1 in BRCA-Proficient Triple-Negative Breast Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Article
- An in vivo screen identifies ependymoma oncogenes and tumor-suppressor genes.Nature genetics · 2015Article
- Human histone acetyltransferase 1 (Hat1) acetylates lysine 5 of histone H2A in vivo.Molecular and cellular biochemistry · 2014Article
- AMPK regulates histone H2B O-GlcNAcylation.Nucleic acids research · 2014Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many tumor suppressors play an important role in the DNA damage pathway. Zinc finger protein 668 (ZNF668) has recently been identified as one of the potential tumor suppressors in breast cancer, but its function in DNA damage response is unknown. Herein, we report that ZNF668 is a regulator of DNA repair. ZNF668 knockdown impairs cell survival after DNA damage without affecting the ATM/ATR DNA-damage signaling cascade. However, recruitment of repair proteins to DNA lesions is decreased. In response to IR, ZNF668 knockdown reduces Tip60-H2AX interaction and impairs IR-induced histone H2AX hyperacetylation, thus impairing chromatin relaxation. Impaired chromatin relaxation causes decreased recruitment of repair proteins to DNA lesions, defective homologous recombination (HR) repair and impaired cell survival after IR. In addition, ZNF668 knockdown decreased RPA phosphorylation and its recruitment to DNA damage foci in response to UV. In both IR and UV damage responses, chromatin relaxation counteracted the impaired loading of repair proteins and DNA repair defects in ZNF668-deficient U2OS cells, indicating that impeded chromatin accessibility at sites of DNA breaks caused the DNA repair defects observed in the absence of ZNF668. Our findings suggest that ZNF668 is a key molecule that links chromatin relaxation with DNA damage response in DNA repair control.
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