ArticleNucleic acids research2015
Modulation of LSD1 phosphorylation by CK2/WIP1 regulates RNF168-dependent 53BP1 recruitment in response to DNA damage.
Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.
- Meta-analysis of cellular phosphoproteome datasets exploring phospho-signaling associated with the RNA-binding protein RAVER1.Scientific reports · 2026Pooled it
- Verapamil Reduces Collagen Synthesis to Alleviate Ureteral Scar Formation by Inhibiting KDM1A-Mediated Epigenetic Silencing of SESN2.Kidney & blood pressure research · 2026Article
- The multifaceted role of post-translational modifications of LSD1 in cellular processes and disease pathogenesis.Genes & diseases · 2025Review
- KDM1A epigenetically enhances RAD51 expression to suppress the STING-associated anti-tumor immunity in esophageal squamous cell carcinoma.Cell death & disease · 2024Article
- Article
- Dual targeting of KDM1A and antioxidants is an effective anticancer strategy.bioRxiv : the preprint server for biology · 2024Article
- Strategies that regulate LSD1 for novel therapeutics.Acta pharmaceutica Sinica. B · 2024Review
- PTEN-mediated dephosphorylation of 53BP1 confers cellular resistance to DNA damage in cancer cells.Molecular oncology · 2024Article
- Article
- Repression of LSD1 potentiates homologous recombination-proficient ovarian cancer to PARP inhibitors through down-regulation of BRCA1/2 and RAD51.Nature communications · 2023Article
- ATM-ESCO2-SMC3 axis promotes 53BP1 recruitment in response to DNA damage and safeguards genome integrity by stabilizing cohesin complex.Nucleic acids research · 2023Article
- LSD1: an emerging face in altering the tumor microenvironment and enhancing immune checkpoint therapy.Journal of biomedical science · 2023Review
- Lysine-specific histone demethylase 1A (KDM1A/LSD1) inhibition attenuates DNA double-strand break repair and augments the efficacy of temozolomide in glioblastoma.Neuro-oncology · 2023Article
- Targeting lysine-specific demethylase 1 (KDM1A/LSD1) impairs colorectal cancer tumorigenesis by affecting cancer cells stemness, motility, and differentiation.Cell death discovery · 2023Article
- Protein kinase CK2 - diverse roles in cancer cell biology and therapeutic promise.Molecular and cellular biochemistry · 2023Review
- Phosphoproteomic analysis on ovarian follicles reveals the involvement of LSD1 phosphorylation in Chicken follicle selection.BMC genomics · 2023Article
- Deubiquitinase OTUD6A promotes breast cancer progression by increasing TopBP1 stability and rendering tumor cells resistant to DNA-damaging therapy.Cell death and differentiation · 2022Article
- PPM1D in Solid and Hematologic Malignancies: Friend and Foe?Molecular cancer research : MCR · 2022Article
- UBE3D Is Involved in Blue Light-Induced Retinal Damage by Regulating Double-Strand Break Repair.Investigative ophthalmology & visual science · 2022Article
- Epigenetics, DNA damage, and aging.The Journal of clinical investigation · 2022Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proper DNA damage response is essential for the maintenance of genome integrity. The E3 ligase RNF168 deficiency fully prevents both the initial recruitment and retention of 53BP1 at sites of DNA damage. In response to DNA damage, RNF168-dependent recruitment of the lysine-specific demethylase LSD1 to the site of DNA damage promotes local H3K4me2 demethylation and ubiquitination of H2A/H2AX, facilitating 53BP1 recruitment to sites of DNA damage. Alternatively, RNF168-mediated K63-linked ubiquitylation of 53BP1 is required for the initial recruitment of 53BP1 to sites of DNA damage and for its function in repair. We demonstrated here that phosphorylation and dephosphorylation of LSD1 at S131 and S137 was mediated by casein kinase 2 (CK2) and wild-type p53-induced phosphatase 1 (WIP1), respectively. LSD1, RNF168 and 53BP1 interacted with each other directly. CK2-mediated phosphorylation of LSD1 exhibited no impact on its interaction with 53BP1, but promoted its interaction with RNF168 and RNF168-dependent 53BP1 ubiquitination and subsequent recruitment to the DNA damage sites. Furthermore, overexpression of phosphorylation-defective mutants failed to restore LSD1 depletion-induced cellular sensitivity to DNA damage. Taken together, our results suggest that LSD1 phosphorylation modulated by CK2/WIP1 regulates RNF168-dependent 53BP1 recruitment directly in response to DNA damage and cellular sensitivity to DNA damaging agents.
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