ArticleNucleic acids research2015
Significance of ligand interactions involving Hop2-Mnd1 and the RAD51 and DMC1 recombinases in homologous DNA repair and XX ovarian dysgenesis.
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 35 papers.
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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
35 citing papers in PubMed, 55 citations in OpenAlex.
- MND1 reduces breast cancer chemosensitivity by promoting RAD51-mediated homologous recombination repair.Cell death & disease · 2026Article
- Breast Cancer Is Increased in Women With Primary Ovarian Insufficiency.The Journal of clinical endocrinology and metabolism · 2025Article
- Hop2-Mnd1 functions as a DNA sequence fidelity switch in Dmc1-mediated DNA recombination.Nature communications · 2024Article
- DSS1 restrains BRCA2's engagement with dsDNA for homologous recombination, replication fork protection, and R-loop homeostasis.Nature communications · 2024Article
- FIGNL1-FIRRM is essential for meiotic recombination and prevents DNA damage-independent RAD51 and DMC1 loading.Nature communications · 2024Article
- H3.1K27me1 loss confers Arabidopsis resistance to Geminivirus by sequestering DNA repair proteins onto host genome.Nature communications · 2023Article
- Identification of a missense variant of MND1 in meiotic arrest and non-obstructive azoospermia.Journal of human genetics · 2023Article
- Crucial roles of the BRCA1-BARD1 E3 ubiquitin ligase activity in homology-directed DNA repair.Molecular cell · 2023Article
- MND1 enables homologous recombination in somatic cells primarily outside the context of replication.Molecular oncology · 2023Article
- The Hop2-Mnd1 Complex and Its Regulation of Homologous Recombination.Biomolecules · 2023Review
- Selected Genetic Factors Associated with Primary Ovarian Insufficiency.International journal of molecular sciences · 2023Review
- The role of bivalent ions in the regulation of D-loop extension mediated by DMC1 during meiotic recombination.iScience · 2022Article
- Biallelic mutations in PSMC3IP are associated with secondary amenorrhea: expanding the spectrum of premature ovarian insufficiency.Journal of assisted reproduction and genetics · 2022Article
- Meiotic Genes and DNA Double Strand Break Repair in Cancer.Frontiers in genetics · 2022Review
- DNA Repair Pathway Choices in CRISPR-Cas9-Mediated Genome Editing.Trends in genetics : TIG · 2021Review
- Genetic network and gene set enrichment analyses identify MND1 as potential diagnostic and therapeutic target gene for lung adenocarcinoma.Scientific reports · 2021Article
- Genetics of Azoospermia.International journal of molecular sciences · 2021Review
- Meiotic Recombination Defects and Premature Ovarian Insufficiency.Frontiers in cell and developmental biology · 2021Review
- Two auxiliary factors promote Dmc1-driven DNA strand exchange via stepwise mechanisms.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Primary ovarian insufficiency, meiosis and DNA repair.Biomedical journal · 2020Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The evolutionarily conserved Hop2-Mnd1 complex is a key cofactor for the meiosis-specific recombinase Dmc1. However, emerging evidence has revealed that Hop2-Mnd1 is expressed in somatic tissues, primary human fibroblasts and cell lines, and that it functions in conjunction with the Rad51 recombinase to repair damaged telomeres via the alternate lengthening of telomeres mechanism. Here, we reveal how distinct DNA-binding activities of Hop2-Mnd1 mediate the stabilization of the RAD51-ssDNA presynaptic filament or stimulate the homologous DNA pairing reaction. We have also endeavored to define the interface that governs the assembly of the higher order complex of Hop2-Mnd1 with RAD51. Unexpectedly, we find that ATP enhances the interaction between Hop2-Mnd1 and RAD51, and that both Hop2 and Mnd1 are involved in RAD51 interaction via their C-terminal regions. Importantly, mutations introduced into these Hop2 and Mnd1 domains, including the HOP2 p.del201Glu mutation present in a patient of XX ovarian dysgenesis, diminish the association and functional synergy of Hop2-Mnd1 with both RAD51 and DMC1. Our findings help delineate the intricate manner in which Hop2-Mnd1 engages and functions with RAD51 and DMC1 in mammalian cells and speak to the possible cause of XX ovarian dysgenesis.
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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.