ArticleThe Journal of biological chemistry2011
Chromatin remodeler sucrose nonfermenting 2 homolog (SNF2H) is recruited onto DNA replication origins through interaction with Cdc10 protein-dependent transcript 1 (Cdt1) and promotes pre-replication complex formation.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 50 citations in OpenAlex.
- SMARCA5-mediated chromatin remodeling is required for germinal center formation.The Journal of experimental medicine · 2024Article
- Quantity and quality of minichromosome maintenance protein complexes couple replication licensing to genome integrity.Communications biology · 2024Review
- DNA replication and replication stress response in the context of nuclear architecture.Chromosoma · 2024Review
- Profilin-1 regulates DNA replication forks in a context-dependent fashion by interacting with SNF2H and BOD1L.Nature communications · 2022Article
- The consequences of differential origin licensing dynamics in distinct chromatin environments.Nucleic acids research · 2022Article
- WASHC1 interacts with MCM2-7 complex to promote cell survival under replication stress.Molecular biology reports · 2022Article
- Inhibition ofInternational journal of molecular sciences · 2022Article
- Article
- TRF2-mediated ORC recruitment underlies telomere stability upon DNA replication stress.Nucleic acids research · 2021Article
- Efficiency and equity in origin licensing to ensure complete DNA replication.Biochemical Society transactions · 2021Review
- BAZ1B the Protean Protein.Genes · 2021Review
- Article
- SLX4-XPF mediates DNA damage responses to replication stress induced by DNA-protein interactions.The Journal of cell biology · 2021Article
- Review
- Mapping the kinetochore MAP functions required for stabilizing microtubule attachments to chromosomes during metaphase.Cytoskeleton (Hoboken, N.J.) · 2019Review
- Review
- Regulation of the initiation of DNA replication in human cells.DNA repair · 2018Review
- Genome-wide analysis of the spatiotemporal regulation of firing and dormant replication origins in human cells.Nucleic acids research · 2018Article
- Myst2/Kat7 histone acetyltransferase interaction proteomics reveals tumour-suppressor Niam as a novel binding partner in embryonic stem cells.Scientific reports · 2017Article
- Regulation and Function of Cdt1; A Key Factor in Cell Proliferation and Genome Stability.Genes · 2016Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
From late mitosis to the G(1) phase of the cell cycle, ORC, CDC6, and Cdt1 form the machinery necessary to load MCM2-7 complexes onto DNA. Here, we show that SNF2H, a member of the ATP-dependent chromatin-remodeling complex, is recruited onto DNA replication origins in human cells in a Cdt1-dependent manner and positively regulates MCM loading. SNF2H physically interacted with Cdt1. ChIP assays indicated that SNF2H associates with replication origins specifically during the G(1) phase. Binding of SNF2H at origins was decreased by Cdt1 silencing and, conversely, enhanced by Cdt1 overexpression. Furthermore, SNF2H silencing prevented MCM loading at origins and moderately inhibited S phase progression. Although neither SNF2H overexpression nor SNF2H silencing appeared to impact rereplication induced by Cdt1 overexpression, Cdt1-induced checkpoint activation was inhibited by SNF2H silencing. Collectively, these data suggest that SNF2H may promote MCM loading at DNA replication origins via interaction with Cdt1 in human cells. Because efficient loading of excess MCM complexes is thought to be required for cells to tolerate replication stress, Cdt1- and SNF2H-mediated promotion of MCM loading may be biologically relevant for the regulation of DNA replication.
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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.