ArticleNature communications2019
MDC1 PST-repeat region promotes histone H2AX-independent chromatin association and DNA damage tolerance.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.
- Epigenome-wide Association Study Shows Differential DNA Methylation of MDC1, KLF9, and CUTA in Autoimmune Thyroid Disease.The Journal of clinical endocrinology and metabolism · 2024Pooled it
- Dynamic chromatin tethering of MDC1 regulates genome stability.Nucleic acids research · 2026Article
- USP18 promotes nasopharyngeal carcinoma radioresistance via TRIM29 oligomerization and ubiquitination.Cell death and differentiation · 2026Article
- Novel driver gene MDC1 confers homologous recombination repair deficiency and genomic instability in chemoresistant relapsing ovarian cancer.Journal of translational medicine · 2026Article
- MDC1 counteracts replication fork reversal and mediates chemosensitivity in BRCA1/2-deficient tumors.Oncogene · 2026Article
- Targeting ATR-CHK1 and ATM-CHK2 Axes in Pancreatic Cancer-A Comprehensive Review of Literature.International journal of molecular sciences · 2026Review
- DNA-damage dependent isoform switching modulates RIF1 DNA repair complex assembly and phase separation.The Journal of biological chemistry · 2025Article
- Structural insights into γH2Ax containing nucleosomes.Nucleic acids research · 2025Article
- Comprehensive identification of proteins interacting with long non-coding RNA TUG1 in R-loop regulation.Journal of biochemistry · 2025Article
- A cancer persistent DNA repair circuit driven by MDM2, MDM4 (MDMX), and mutant p53 for recruitment of MDC1 and 53BP1 on chromatin.Nucleic acids research · 2025Article
- Histone Phosphorylation in DNA Damage Response.International journal of molecular sciences · 2025Review
- The PST repeat region of MDC1 is a tunable multivalent chromatin tethering domain.bioRxiv : the preprint server for biology · 2025Article
- Cuproptosis-related genes and agents: implications in tumor drug resistance and future perspectives.Frontiers in pharmacology · 2025Review
- The N-terminal region of DNMT3A engages the nucleosome surface to aid chromatin recruitment.EMBO reports · 2024Article
- Diffusion of activated ATM explains γH2AX and MDC1 spread beyond the DNA damage site.iScience · 2024Article
- Evolved histone tail regulates 53BP1 recruitment at damaged chromatin.Nature communications · 2024Article
- Ki-67 is necessary during DNA replication for fork protection and genome stability.Genome biology · 2024Article
- Identification of plants' functional counterpart of the metazoan mediator of DNA Damage checkpoint 1.EMBO reports · 2024Article
- Aldolase A promotes cervical cancer cell radioresistance by regulating the glycolysis and DNA damage after irradiation.Cancer biology & therapy · 2023Article
- GSE1 links the HDAC1/CoREST co-repressor complex to DNA damage.Nucleic acids research · 2023Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Histone H2AX and MDC1 are key DNA repair and DNA-damage signalling proteins. When DNA double-strand breaks (DSBs) occur, H2AX is phosphorylated and then recruits MDC1, which in turn serves as a docking platform to promote the localization of other factors, including 53BP1, to DSB sites. Here, by using CRISPR-Cas9 engineered human cell lines, we identify a hitherto unknown, H2AX-independent, function of MDC1 mediated by its PST-repeat region. We show that the PST-repeat region directly interacts with chromatin via the nucleosome acidic patch and mediates DNA damage-independent association of MDC1 with chromatin. We find that this region is largely functionally dispensable when the canonical γH2AX-MDC1 pathway is operative but becomes critical for 53BP1 recruitment to DNA-damage sites and cell survival following DSB induction when H2AX is not available. Consequently, our results suggest a role for MDC1 in activating the DDR in areas of the genome lacking or depleted of H2AX.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.