ArticleThe Journal of biological chemistry
Motifs of the C-terminal domain of MCM9 direct localization to sites of mitomycin-C damage for RAD51 recruitment.
Article in The Journal of biological chemistry. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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Who cites it
22 citing papers in PubMed, 30 citations in OpenAlex.
- Structural Activation of DNA Unwinding by MCM8/9/HROB.bioRxiv : the preprint server for biology · 2026Article
- Dissecting the shared genetic architecture between testosterone traits and attention-deficit/hyperactivity disorder.European child & adolescent psychiatry · 2026Article
- Critical roles of MCM8 in meiotic recombination during mouse spermatogenesis.bioRxiv : the preprint server for biology · 2026Article
- MCM8-9 helicase activity protects primordial germ cell development to prevent premature ovarian insufficiency.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- MCM8/9 and FANCD2 interact within a shared pathway in response to replication stress caused by DNA crosslinks.DNA repair · 2025Article
- AmNA-Modified Antisense Oligonucleotide Targeting MCM8 as a Cancer-Specific Chemosensitizer for Platinum Compounds.Cancer science · 2025Article
- Review
- HROB Is Implicated in DNA Replication.Genes · 2024Article
- MCM9 compound heterozygosity in an adolescent with premature ovarian insufficiency.Endocrinology, diabetes & metabolism case reports · 2024Article
- DMC1 and RAD51 bind FxxA and FxPP motifs of BRCA2 via two separate interfaces.Nucleic acids research · 2024Article
- MCM8 promotes gastric cancer progression through RPS15A and predicts poor prognosis.Cancer medicine · 2024Article
- Mechanism of DNA unwinding by MCM8-9 in complex with HROB.Nature communications · 2024Article
- Activity, substrate preference and structure of the HsMCM8/9 helicase.Nucleic acids research · 2023Article
- Article
- Mechanism of DNA unwinding by hexameric MCM8-9 in complex with HROB.Research square · 2023Article
- Review
- Review
- Decorin evokes reversible mitochondrial depolarization in carcinoma and vascular endothelial cells.American journal of physiology. Cell physiology · 2022Article
- A multi-functional role for the MCM8/9 helicase complex in maintaining fork integrity during replication stress.Nature communications · 2022Article
- Gerontology through the Eyes of 21st Century Toxicology.Chemical research in toxicology · 2022Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
The MCM8/9 complex is implicated in aiding fork progression and facilitating homologous recombination (HR) in response to several DNA damage agents. MCM9 itself is an outlier within the MCM family containing a long C-terminal extension (CTE) comprising 42% of the total length, but with no known functional components and high predicted disorder. In this report, we identify and characterize two unique motifs within the primarily unstructured CTE that are required for localization of MCM8/9 to sites of mitomycin C (MMC)-induced DNA damage. First, an unconventional "bipartite-like" nuclear localization (NLS) motif consisting of two positively charged amino acid stretches separated by a long intervening sequence is required for the nuclear import of both MCM8 and MCM9. Second, a variant of the BRC motif (BRCv) similar to that found in other HR helicases is necessary for localization to sites of MMC damage. The MCM9-BRCv directly interacts with and recruits RAD51 downstream to MMC-induced damage to aid in DNA repair. Patient lymphocytes devoid of functional MCM9 and discrete MCM9 knockout cells have a significantly impaired ability to form RAD51 foci after MMC treatment. Therefore, the disordered CTE in MCM9 is functionally important in promoting MCM8/9 activity and in recruiting downstream interactors; thus, requiring full-length MCM9 for proper DNA repair.
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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.