ArticleLife science alliance2019
Human CST suppresses origin licensing and promotes AND-1/Ctf4 chromatin association.
Article in Life science alliance, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 35 citations in OpenAlex.
- Conditional deletion of human STN1 leads to telomere dysfunction, genome instability and proliferation defects.Journal of cell science · 2026Article
- Article
- Dysfunction of Telomeric Cdc13-Stn1-Ten1 Simultaneously Activates DNA Damage and Spindle Checkpoints.Cells · 2024Article
- Progerin Can Induce DNA Damage in the Absence of Global Changes in Replication or Cell Proliferation.bioRxiv : the preprint server for biology · 2024Article
- Human CST complex restricts excessive PrimPol repriming upon UV induced replication stress by suppressing p21.Nucleic acids research · 2024Article
- Conditional Depletion of STN1 in Mouse Embryonic Fibroblasts.Bio-protocol · 2024Article
- Guardians of the Genome: How the Single-Stranded DNA-Binding Proteins RPA and CST Facilitate Telomere Replication.Biomolecules · 2024Review
- Progerin can induce DNA damage in the absence of global changes in replication or cell proliferation.PloS one · 2024Article
- Pot1 promotes telomere DNA replication via the Stn1-Ten1 complex in fission yeast.Nucleic acids research · 2023Article
- CaMKK2 and CHK1 phosphorylate human STN1 in response to replication stress to protect stalled forks from aberrant resection.Nature communications · 2023Article
- Cooperative interaction of CST and RECQ4 resolves G-quadruplexes and maintains telomere stability.EMBO reports · 2023Article
- RPA engages telomeric G-quadruplexes more effectively than CST.Nucleic acids research · 2023Article
- Yeast Stn1 promotes MCM to circumvent Rad53 control of the S phase checkpoint.Current genetics · 2022Article
- The yeast Dbf4 ZnCurrent genetics · 2022Article
- Pan-Cancer Analyses Identify the CTC1-STN1-TEN1 Complex as a Protective Factor and Predictive Biomarker for Immune Checkpoint Blockade in Cancer.Frontiers in genetics · 2022Article
- Telomeres and Cancer.Life (Basel, Switzerland) · 2021Review
- Crosstalk between CST and RPA regulates RAD51 activity during replication stress.Nature communications · 2021Article
- Fission yeast Stn1 maintains stability of repetitive DNA at subtelomere and ribosomal DNA regions.Nucleic acids research · 2021Article
- OB-Folds and Genome Maintenance: Targeting Protein-DNA Interactions for Cancer Therapy.Cancers · 2021Review
- CST in maintaining genome stability: Beyond telomeres.DNA repair · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Human CTC1-STN1-TEN1 (CST) is an RPA-like single-stranded DNA-binding protein that interacts with DNA polymerase α-primase (pol α) and functions in telomere replication. Previous studies suggest that CST also promotes replication restart after fork stalling. However, the precise role of CST in genome-wide replication remains unclear. In this study, we sought to understand whether CST alters origin licensing and activation. Replication origins are licensed by loading of the minichromosome maintenance 2-7 (MCM) complex in G1 followed by replisome assembly and origin firing in S-phase. We find that CST directly interacts with the MCM complex and disrupts binding of CDT1 to MCM, leading to decreased origin licensing. We also show that CST enhances replisome assembly by promoting AND-1/pol α chromatin association. Moreover, these interactions are not dependent on exogenous replication stress, suggesting that CST acts as a specialized replication factor during normal replication. Overall, our findings implicate CST as a novel regulator of origin licensing and replisome assembly/fork progression through interactions with MCM, AND-1, and pol α.
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What OpenQuestion holds
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.