ArticleEMBO reports2017
Human RIF1 and protein phosphatase 1 stimulate DNA replication origin licensing but suppress origin activation.
Article in EMBO reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.
What it found
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Who cites it
94 citing papers in PubMed, 149 citations in OpenAlex.
- Nuclear compartmentalization at the G1/S transition plays a key role in DNA replication control.Nature communications · 2026Article
- CDC7 and APC/CNature communications · 2026Article
- Exploring the multifaceted Dbf4-dependent kinase from temporal, spatial, and substrate repertoire perspectives.Communications biology · 2026Review
- Adaptive Replication Fork Acceleration by CDK1-Cyclin B1 Sustains Genome Duplication despite Impaired Origin Firing.bioRxiv : the preprint server for biology · 2026Article
- Chromosome fusion enhances dependency on Rif1 for entanglement resolution during meiosis in S. pombe.Communications biology · 2026Article
- Transcription elongation can be sufficient, but is not necessary, to advance replication timing.EMBO reports · 2026Article
- FANCD2 restrains fork progression and prevents fragility at early origins upon re-replication.Nature communications · 2026Article
- Regulated TRESLIN-MTBP loading governs initiation zones and replication timing in human DNA replication.Nature communications · 2025Article
- DNA-damage dependent isoform switching modulates RIF1 DNA repair complex assembly and phase separation.The Journal of biological chemistry · 2025Article
- Centromere protection requires strict mitotic inactivation of the Bloom syndrome helicase complex.Nature communications · 2025Article
- Replication-dependent histone labeling dissects the physical properties of euchromatin/heterochromatin in living human cells.Science advances · 2025Article
- R-loops acted on by RNase H1 influence DNA replication timing and genome stability in Leishmania.Nature communications · 2025Article
- Transcription can be sufficient, but is not necessary, to advance replication timing.bioRxiv : the preprint server for biology · 2025Article
- A multiplicative behavioral model of DNA replication initiation in cells.Open life sciences · 2025Article
- Roles for the 3D genome in the cell cycle, DNA replication, and double strand break repair.Frontiers in cell and developmental biology · 2025Review
- Review
- DBF4, not DRF1, is the crucial regulator of CDC7 kinase at replication forks.The Journal of cell biology · 2024Article
- Dynamics of Replication-Associated Protein Levels through the Cell Cycle.International journal of molecular sciences · 2024Article
- Fate of telomere entanglements is dictated by the timing of anaphase midregion nuclear envelope breakdown.Nature communications · 2024Article
- Bioactive nutraceuticals as G4 stabilizers: potential cancer prevention and therapy-a critical review.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
34 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
The human RIF1 protein controls DNA replication, but the molecular mechanism is largely unknown. Here, we demonstrate that human RIF1 negatively regulates DNA replication by forming a complex with protein phosphatase 1 (PP1) that limits phosphorylation-mediated activation of the MCM replicative helicase. We identify specific residues on four MCM helicase subunits that show hyperphosphorylation upon RIF1 depletion, with the regulatory N-terminal domain of MCM4 being particularly strongly affected. In addition to this role in limiting origin activation, we discover an unexpected new role for human RIF1-PP1 in mediating efficient origin licensing. Specifically, during the G1 phase of the cell cycle, RIF1-PP1 protects the origin-binding ORC1 protein from untimely phosphorylation and consequent degradation by the proteasome. Depletion of RIF1 or inhibition of PP1 destabilizes ORC1, thereby reducing origin licensing. Consistent with reduced origin licensing, RIF1-depleted cells exhibit increased spacing between active origins. Human RIF1 therefore acts as a PP1-targeting subunit that regulates DNA replication positively by stimulating the origin licensing step, and then negatively by counteracting replication origin activation.
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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.