ArticleCell cycle (Georgetown, Tex.)2014
Human CST abundance determines recovery from diverse forms of DNA damage and replication stress.
Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 55 citations in OpenAlex.
- Stn1 promotes zebrafish oocyte development via amplifying Wnt/β-catenin signaling.EMBO reports · 2026Article
- KRAS-induced STN1 (OBFC1) promotes proper CTC1-STN1-TEN1 complex-independent DNA double-strand break repair and cell cycle checkpoint maintenance in pancreatic cancer.Nucleic acids research · 2025Article
- Suppression of CTC1 inhibits hepatocellular carcinoma cell growth and enhances RHPS4 cytotoxicity.Molecular biology reports · 2024Article
- Survival-Related Genes on Chromosomes 6 and 17 in Medulloblastoma.International journal of molecular sciences · 2024Article
- Human CST complex restricts excessive PrimPol repriming upon UV induced replication stress by suppressing p21.Nucleic acids research · 2024Article
- Guardians of the Genome: How the Single-Stranded DNA-Binding Proteins RPA and CST Facilitate Telomere Replication.Biomolecules · 2024Review
- 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
- Deficiency in mammalian STN1 promotes colon cancer development via inhibiting DNA repair.Science advances · 2023Article
- Article
- Transcriptomic Analysis of Conserved Telomere Maintenance Component 1 (CTC1) and Its Association with Leukemia.Journal of clinical medicine · 2022Article
- Yeast Stn1 promotes MCM to circumvent Rad53 control of the S phase checkpoint.Current genetics · 2022Article
- Telomeres and Cancer.Life (Basel, Switzerland) · 2021Review
- Crosstalk between CST and RPA regulates RAD51 activity during replication stress.Nature communications · 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
- Shaping human telomeres: from shelterin and CST complexes to telomeric chromatin organization.Nature reviews. Molecular cell biology · 2021Review
- Article
- The structure of human CST reveals a decameric assembly bound to telomeric DNA.Science (New York, N.Y.) · 2020Article
- Roles of OB-Fold Proteins in Replication Stress.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
Mammalian CST (CTC1-STN1-TEN1) is a telomere-associated complex that functions in telomere duplex replication and fill-in synthesis of the telomeric C-strand following telomerase action. CST also facilitates genome-wide replication recovery after HU-induced fork stalling by increasing origin firing. CTC1 and STN1 were originally isolated as a DNA polymerase α stimulatory factor. Here we explore how CST abundance affects recovery from drugs that cause different types of DNA damage and replication stress. We show that recovery from HU and aphidicolin induced replication stress is increased by CST over-expression. Elevated CST increases dNTP incorporation and origin firing after HU release and decreases the incidence of anaphase bridges and micronuclei after aphidicolin removal. While the frequency of origin firing after HU release is proportional to CST abundance, the number of cells entering S-phase to initiate replication is unchanged by CST overexpression or STN1 depletion. Instead the CST-related changes in origin firing take place in cells that were already in S-phase at the time of HU addition, indicating that CST modulates firing of late or dormant origins. CST abundance also influences cell viability after treatment with HU, aphidicolin, MMS and camptothecin. Viability is increased by elevated CST and decreased by STN1 depletion, indicating that endogenous CST levels are limiting. However, CST abundance does not affect viability after MMC treatment. Thus, CST facilitates recovery from many, but not all, forms of exogenous DNA damage. Overall our results suggest that CST is needed in stoichiometric amounts to facilitate re-initiation of DNA replication at repaired forks and/or dormant origins.
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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.