Affinage

CTC1

CST complex subunit CTC1 · UniProt Q2NKJ3

Length
1217 aa
Mass
134.6 kDa
Annotated
2026-06-09
43 papers in source corpus 16 papers cited in narrative 16 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/7 claims corpus-supported (86%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CTC1 is the largest subunit of the heterotrimeric, RPA-like CST complex (CTC1-STN1-TEN1) that binds single-stranded DNA with high, sequence-independent affinity and acts at telomeres to coordinate the completion of replication and the regulation of telomerase (PMID:19854130, PMID:30026550). Mechanistically, CST stimulates DNA polymerase α-primase to prime and fill in the telomeric C-strand: it functions at the priming step on ssDNA templates (PMID:22086929), operates as the α-accessory factor that stimulates pol α-primase activity (PMID:22267198), and promotes restart of stalled replication forks during telomere replication, with loss causing C-strand depletion, excess G-strand ssDNA, ATR-dependent checkpoint activation, and catastrophic telomere loss (PMID:22531781, PMID:28334750). CST balances this fill-in activity against telomerase: CTC1-STN1 binding terminates telomerase-mediated G-strand extension and prevents overhang overextension, while the CTC1 OB-B domain mediates a TPP1 interaction that is the key determinant of telomerase termination, separable from its C-strand synthesis role (PMID:30026550, PMID:37021555). Beyond telomeres, CST acts as a central component of the 53BP1 axis at double-strand breaks, suppressing EXO1- and BLM-DNA2-mediated end resection to govern repair pathway choice, with BRCA1-BARD1 relieving the CST-imposed EXO1 blockade (PMID:40403056). CST also localizes to ALT-associated PML bodies and restrains telomeric recombination in ALT cancer cells (PMID:28366536), and CTC1 interacts with RAD51 to protect GC-rich genomic fragile sites against replication-stress-induced breakage (PMID:29481669). CTC1 stability is set by STN1, which binds near the OB-G cleft and competes with TRIM32-mediated ubiquitination and proteasomal degradation (PMID:40923710). Pathogenic CTC1 mutations in Coats plus disrupt CST assembly, pol α-primase interaction, ssDNA binding, nuclear accumulation, and/or telomere association, producing internal telomeric ssDNA gaps, telomere shortening, chromosome fusions, and global genome instability (PMID:22267198, PMID:24115768, PMID:23869908).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2009 High

    Established that mammalian CTC1 is not a standalone factor but a subunit of an RPA-like ssDNA-binding trimer (CST) acting at telomeres, defining the molecular entity to be studied.

    Evidence Protein isolation, ssDNA binding assays, IF colocalization, and STN1 knockdown with telomere analysis

    PMID:19854130

    Open questions at the time
    • Did not define which enzymatic step CST controls
    • Fraction of telomeres bound and cell-cycle dependence not mechanistically explained
  2. 2011 High

    Placed CST at the priming step of DNA synthesis, showing it regulates DNA pol α-primase rather than elongation, the first mechanistic assignment of a catalytic function.

    Evidence Xenopus egg extract reconstitution with xStn1 immunodepletion and primed vs unprimed ssDNA controls

    PMID:22086929

    Open questions at the time
    • Done in Xenopus extract, not human reconstitution
    • Direct physical contact between CTC1 and pol α not mapped here
  3. 2012 Medium

    Connected CTC1 to human disease and to pol α-primase stimulation, showing loss-of-function causes telomere shortening and DNA damage in patients.

    Evidence Coats plus patient mutation analysis, telomere length and γH2AX immunostaining in patient cells; biochemical identification as α-accessory factor

    PMID:22267198

    Open questions at the time
    • Single study
    • Did not separate replication defect from telomerase dysregulation
  4. 2012 High

    Defined CTC1's in vivo role as facilitating telomere replication via stalled fork restart, distinct from telomere capping, and linked its loss to ATR checkpoint and bone marrow failure.

    Evidence Conditional mouse knockout with telomere FISH, BrdU incorporation, flow cytometry, ATR pathway analysis

    PMID:22531781

    Open questions at the time
    • Mechanism of fork restart not biochemically reconstituted
    • Relationship between leading C-strand loss and pol α stimulation not resolved
  5. 2013 High

    Resolved how disease mutations act by mapping them to discrete molecular defects—complex assembly, pol α binding, ssDNA binding, nuclear localization, telomere association—unifying genotype with telomere replication failure.

    Evidence Co-IP, in vitro ssDNA binding, IF, telomere FISH across disease and active-site mutation panels in human cells

    PMID:23869908 PMID:24115768

    Open questions at the time
    • Some mutations had pleiotropic effects, complicating one-to-one defect assignment
    • STN1 stability effects characterized only in part
  6. 2017 High

    Demonstrated that CST-mediated C-strand fill-in is as essential as telomerase G-strand extension for length maintenance, establishing the two-step balance at the heart of telomere homeostasis.

    Evidence CTC1 disruption in human cells with overhang assays, RPA ChIP, and time-course telomere length measurement

    PMID:28334750

    Open questions at the time
    • Did not identify the domain mediating telomerase termination
    • Coupling between fill-in and telomerase shutoff left mechanistically open
  7. 2017 Medium

    Extended CST function to ALT telomere maintenance, showing it localizes to APBs and restrains telomeric recombination.

    Evidence IF colocalization in ALT cells, CST knockdown, C-circle assay, telomere FISH

    PMID:28366536

    Open questions at the time
    • Direct partners at APBs not identified
    • Single lab
  8. 2018 High

    Dissected the contributions of individual subunits and a central OB-fold, showing CTC1-STN1 is sufficient to terminate telomerase while TEN1 stabilizes ssDNA engagement for C-strand synthesis, and that pol α binding is required to fully repress telomerase.

    Evidence Crystal structure of CTC1 OB-fold; CRISPR knockouts of individual subunits; CRISPR knock-in of CTC1 L1142H; Co-IP, ssDNA binding, overhang and telomerase recruitment assays

    PMID:29228254 PMID:29774655 PMID:30026550

    Open questions at the time
    • Full-length CST structure not determined
    • TPP1 not yet implicated as the termination partner
  9. 2018 Medium

    Revealed a non-telomeric genome-protection role, mapping a RAD51-interacting region of CTC1 that guards GC-rich fragile sites against replication-stress-induced breakage.

    Evidence CST-RAD51 Co-IP, RAD51 foci IF, chromosome breakage and fragile-site FISH across a disease mutation panel

    PMID:29481669

    Open questions at the time
    • RAD51 interaction not reconstituted in vitro
    • Relationship to canonical HR recombination unclear
  10. 2020 Medium

    Showed CTC1 loss produces a local but not global ATR checkpoint, attributable to reduced TopBP1, refining how telomere-localized damage signals propagate.

    Evidence Conditional CTC1 knockout with phospho-CHK1/RPA/ATR immunoblot, TopBP1 levels, and ATR/CHK1/ATM inhibition epistasis

    PMID:33269665

    Open questions at the time
    • Mechanism linking CTC1 loss to TopBP1 reduction unknown
    • Single lab
  11. 2023 High

    Identified the CTC1 OB-B domain–TPP1 interaction as the specific molecular switch for telomerase termination, cleanly separating this function from C-strand fill-in.

    Evidence CTC1 domain deletion and point mutant panel in CTC1-/- cells, CST-TPP1 Co-IP, telomerase ChIP, C-strand fill-in assays

    PMID:37021555

    Open questions at the time
    • Structural basis of the CTC1-TPP1 interface not resolved
    • How TPP1 binding triggers telomerase release mechanistically unclear
  12. 2025 High

    Defined CST as a central 53BP1-axis effector at double-strand breaks that suppresses EXO1 and BLM-DNA2 resection to control repair pathway choice, linking CST mutants to PARP inhibitor resistance.

    Evidence Epistasis genetics, resection assays, CST DNA-binding and interaction mutants, in vitro resection reconstitution, PARP inhibitor sensitivity in BRCA1-deficient cells

    PMID:40403056

    Open questions at the time
    • How CST is recruited to DSBs versus telomeres not distinguished
    • Stoichiometry with 53BP1 axis components unresolved
  13. 2025 Medium

    Established post-translational control of CTC1 abundance, showing STN1 protects CTC1 from TRIM32-mediated ubiquitination by competing at the OB-G cleft.

    Evidence Reciprocal Co-IP, ubiquitination and proteasome-rescue assays, AlphaFold3 modeling, proliferation assays

    PMID:40923710

    Open questions at the time
    • TRIM32-CTC1 interface validated only by modeling and Co-IP
    • Physiological conditions regulating this competition unknown
    • Not independently replicated

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CST is differentially targeted to telomeres, replication forks, ALT bodies, and DSBs—and how a single ssDNA-binding complex is partitioned among these functions—remains unresolved.
  • No full-length CST structure on substrate
  • Recruitment determinants distinguishing telomeric vs genome-wide roles unknown
  • Regulation of the resection-suppression versus fill-in functions not integrated

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 5 GO:0003677 DNA binding 3 GO:0060090 molecular adaptor activity 2
Localization
GO:0000228 nuclear chromosome 3 GO:0005634 nucleus 1
Pathway
R-HSA-69306 DNA Replication 4 R-HSA-73894 DNA Repair 2 R-HSA-8953897 Cellular responses to stimuli 2
Partners
BLMEXO1RAD51STN1TEN1TPP1TRIM32
Complex memberships
CST complex (CTC1-STN1-TEN1)alpha-accessory factor (AAF) complex

Evidence

Reading pass · 16 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2009 Mammalian CTC1 forms an RPA-like trimeric complex with STN1 and TEN1 (CST complex) that binds single-stranded DNA with high affinity in a sequence-independent manner and associates with a fraction of telomeres throughout the cell cycle. STN1 knockdown caused significant increases in single-stranded G-strand telomeric DNA, indicating a role in DNA metabolism at telomeres. Protein isolation, ssDNA binding assays, immunofluorescence/colocalization, knockdown with telomere analysis Molecular cell High 19854130
2011 Xenopus CST (xCST) complex is involved in priming DNA synthesis on single-stranded DNA templates via regulation of DNA polymerase α-primase; immunodepletion of xStn1 blocked DNA synthesis on ssDNA template but not on pre-primed ssDNA, indicating CST acts at the priming step. Xenopus egg extract reconstitution, immunodepletion of xStn1, in vitro DNA replication assay on ssDNA templates The Journal of biological chemistry High 22086929
2012 CTC1 is a subunit of the α-accessory factor (AAF) complex that stimulates the activity of DNA polymerase-α primase. CTC1 mutations in Coats plus patients result in shortened telomeres and increased spontaneous γH2AX-positive cells. Patient mutation analysis, telomere length measurement, γH2AX immunostaining in patient-derived cell lines Nature genetics Medium 22267198
2012 Conditional deletion of CTC1 in mice leads to ATR-dependent G2/M checkpoint activation, global cellular proliferative defects, bone marrow failure, and catastrophic telomere loss. CTC1 facilitates telomere replication by promoting efficient restart of stalled replication forks, and its deletion causes increased loss of leading C-strand telomeres and accumulation of excessive ssDNA telomere sequences. CTC1 is not required for telomere capping. Conditional mouse knockout (Cre-lox), flow cytometry, telomere FISH, BrdU incorporation, ATR pathway analysis The EMBO journal High 22531781
2013 Disease mutations in CTC1 disrupt: (1) CST complex formation with STN1/TEN1; (2) physical interaction with DNA polymerase α-primase; (3) telomeric ssDNA binding in vitro; (4) nuclear accumulation; and/or (5) telomere association in vivo. All mutations commonly lead to accumulation of internal single-stranded gaps of telomeric DNA, indicating telomere DNA replication defects. Some CTC1 mutations also unleash telomerase repression and telomere length control. Co-immunoprecipitation, in vitro ssDNA binding assays, immunofluorescence, telomere FISH, active-site/disease mutation analysis Genes & development High 24115768
2013 CTC1 frameshift mutations generate truncated or unstable protein products that cannot form a complex with STN1-TEN1 at telomeres, resulting in progressive telomere shortening and chromosome fusions. CTC1 missense mutations can form the CST complex at telomeres but may be repressed by frameshift mutants. CTC1 mutations promote telomere dysfunction by decreasing STN1 stability and reducing STN1's ability to interact with DNA Pol-α. Biochemical characterization of mutant proteins, Co-IP, telomere FISH, chromosomal fusion analysis in human cells Aging cell Medium 23869908
2017 Disruption of CTC1 in human cells results in elongation of the 3′ G-strand overhang, accumulation of RPA at telomeres, and telomeric DNA damage signaling. C-strand length decreases continuously following CTC1 disruption while G-strand initially grows (due to telomerase), indicating CST-mediated C-strand fill-in is essential for telomere length maintenance and that telomerase-mediated G-strand extension and CST-mediated C-strand fill-in are equally important. CTC1 disruption in human cells, telomere overhang assays, RPA ChIP, telomere length measurement over time Nucleic acids research High 28334750
2017 Human CST complex localizes to ALT-associated PML bodies (APBs) in ALT cancer cells. CST suppression in ALT cells induces telomere fragility, elevated telomeric DNA recombination, reduces C-circle and t-circle abundance, and causes multinucleation. IF colocalization in ALT cells, CST knockdown, C-circle assay, telomere FISH Experimental cell research Medium 28366536
2018 Crystal structure of a central OB-fold domain of human CTC1 was determined. This domain does not directly contribute to substrate binding but affects full-length CTC1 localization to telomeres and STN1-TEN1 binding. Disease mutations R840W and V871M contribute to the fold of this domain. Deletion of this OB-fold domain leads to increased telomere length, frequency of internal single G-strands, and fragile telomeres. X-ray crystallography, in vitro binding assays, site-directed mutagenesis, telomere localization assays, telomere FISH Nucleic acids research High 29228254
2018 CTC1-STN1 interaction is required to repress telomerase activity. CTC1^L1142H mutation impairs CTC1-STN1 interaction, leading to telomerase-mediated telomere elongation. Impaired CTC1^L1142H:STN1 interaction with DNA Pol-α results in increased telomerase recruitment and further telomere elongation. CST binding to DNA Pol-α is required to fully repress telomerase activity. CST mutants that fail to interact with DNA Pol-α result in loss of C-strand maintenance and catastrophic telomere shortening. CRISPR/Cas9 knock-in of disease mutation, Co-IP, telomere length analysis, telomerase recruitment assay Aging cell High 29774655
2018 Pathogenic CTC1 missense and small deletion mutations induce spontaneous chromosome breakage and severe chromosome fragmentation elevated by replication stress, leading to global genome instabilities. These mutations abolish or reduce CST interaction with RAD51, disrupt RAD51 foci formation, and/or diminish binding to GC-rich genomic fragile sites. The aa 600-989 region of CTC1 contains a RAD51-interacting domain. Co-IP (CST-RAD51), RAD51 foci immunofluorescence, chromosome breakage analysis, fragile site FISH, disease mutation panel Nucleic acids research Medium 29481669
2018 CTC1-STN1 limits telomerase action to prevent G-overhang overextension. CTC1-/- cells exhibit telomeric DNA damage and growth arrest due to overhang elongation. CTC1-STN1 retains ssDNA binding affinity but TEN1 stabilizes binding. CTC1-STN1 binding is sufficient to terminate telomerase action, but without TEN1 it cannot properly engage DNA polymerase α on the overhang for C-strand synthesis. CRISPR knockout of individual CST subunits (CTC1, TEN1), ssDNA binding assays, telomere overhang analysis, cell proliferation assays Nature communications High 30026550
2020 CTC1 knockout inhibits CHK1 phosphorylation following hydroxyurea-induced replication stress by causing decreased levels of the ATR activator TopBP1. CTC1 KO activates ATR locally at telomeres (leading to RPA and ATR autophosphorylation) but does not elicit a global checkpoint response through CHK1. ATR but not CHK1 or ATM is required for G2 arrest and RPA phosphorylation following CTC1 removal. Conditional CTC1 knockout, phospho-CHK1/RPA/ATR immunoblot, TopBP1 protein level analysis, ATR/CHK1/ATM inhibition epistasis Cell cycle (Georgetown, Tex.) Medium 33269665
2023 CTC1 OB-B domain is a key determinant of telomerase termination but not C-strand synthesis. CTC1-ΔB expression rescues C-strand fill-in and prevents telomeric DNA damage but causes progressive telomere elongation and accumulation of telomerase at telomeres. CTC1 OB-B domain mediates interaction with TPP1, and this CTC1-TPP1 interaction plays a key role in telomerase termination. OB-B point mutations weakening TPP1 association track with inability to limit telomerase action. CTC1 domain deletion/point mutant panel in CTC1-/- cells, Co-IP (CST-TPP1), telomere length analysis, telomerase ChIP, C-strand fill-in assays Nucleic acids research High 37021555
2025 The CST complex suppresses DNA end resection by EXO1 and the BLM-DNA2 helicase-nuclease complex, controlling DSB repair pathway choice between end joining and homologous recombination. CST acts as a central 53BP1 axis component. BRCA1-BARD1 alleviates CST-imposed EXO1 blockade but has little effect on BLM-DNA2 restriction. CST mutants impaired for DNA binding or BLM-EXO1 interaction exhibit hyper-resection and render BRCA1-deficient cells resistant to PARP inhibitors. Epistasis genetics, resection assays, CST DNA-binding and protein interaction mutants, PARP inhibitor sensitivity in BRCA1-deficient cells, in vitro reconstitution of end resection Science (New York, N.Y.) High 40403056
2025 STN1 directly interacts with CTC1 and stabilizes CTC1 by preventing its TRIM32-mediated ubiquitination and proteasomal degradation. TRIM32 interacts with the OB-G domain of CTC1 near the STN1-interacting 'cleft' motif, and STN1 binding to this region competes with TRIM32 to protect CTC1 from degradation. TRIM32 and the CTC1/STN1 complex exert opposing effects on cellular proliferation. Co-IP (STN1-CTC1, TRIM32-CTC1), ubiquitination assays, proteasome inhibitor rescue, AlphaFold3 structural modeling, knockdown/overexpression proliferation assays Aging cell Medium 40923710

Source papers

Stage 0 corpus · 43 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2009 RPA-like mammalian Ctc1-Stn1-Ten1 complex binds to single-stranded DNA and protects telomeres independently of the Pot1 pathway. Molecular cell 286 19854130
2012 Mutations in CTC1, encoding conserved telomere maintenance component 1, cause Coats plus. Nature genetics 228 22267198
2012 Genome-wide meta-analysis points to CTC1 and ZNF676 as genes regulating telomere homeostasis in humans. Human molecular genetics 191 23001564
2012 Mutations in CTC1, encoding the CTS telomere maintenance complex component 1, cause cerebroretinal microangiopathy with calcifications and cysts. American journal of human genetics 144 22387016
2012 CTC1 deletion results in defective telomere replication, leading to catastrophic telomere loss and stem cell exhaustion. The EMBO journal 143 22531781
2012 CTC1 Mutations in a patient with dyskeratosis congenita. Pediatric blood & cancer 108 22532422
2013 Molecular basis of telomere syndrome caused by CTC1 mutations. Genes & development 95 24115768
2017 CTC1-mediated C-strand fill-in is an essential step in telomere length maintenance. Nucleic acids research 81 28334750
2013 Functional characterization of human CTC1 mutations reveals novel mechanisms responsible for the pathogenesis of the telomere disease Coats plus. Aging cell 64 23869908
2018 CTC1-STN1 terminates telomerase while STN1-TEN1 enables C-strand synthesis during telomere replication in colon cancer cells. Nature communications 58 30026550
2011 Xenopus laevis Ctc1-Stn1-Ten1 (xCST) protein complex is involved in priming DNA synthesis on single-stranded DNA template in Xenopus egg extract. The Journal of biological chemistry 57 22086929
2018 CTC1-STN1 coordinates G- and C-strand synthesis to regulate telomere length. Aging cell 43 29774655
2018 Pathogenic CTC1 mutations cause global genome instabilities under replication stress. Nucleic acids research 38 29481669
2017 The human CTC1/STN1/TEN1 complex regulates telomere maintenance in ALT cancer cells. Experimental cell research 34 28366536
2018 CTC1 mutations in a Brazilian family with progeroid features and recurrent bone fractures. Molecular genetics & genomic medicine 26 30393977
2020 A unique case of coats plus syndrome and dyskeratosis congenita in a patient with CTC1 mutations. Ophthalmic genetics 25 32543263
2014 CTC1 increases the radioresistance of human melanoma cells by inhibiting telomere shortening and apoptosis. International journal of molecular medicine 25 24718655
2018 Structural and functional analysis of an OB-fold in human Ctc1 implicated in telomere maintenance and bone marrow syndromes. Nucleic acids research 19 29228254
2015 Whole exome sequencing in an Indian family links Coats plus syndrome and dextrocardia with a homozygous novel CTC1 and a rare HES7 variation. BMC medical genetics 19 25928698
2015 Cerebro-retinal microangiopathy with calcifications and cysts due to recessive mutations in the CTC1 gene. Revue neurologique 18 25843205
2020 Human CTC1 promotes TopBP1 stability and CHK1 phosphorylation in response to telomere dysfunction and global replication stress. Cell cycle (Georgetown, Tex.) 17 33269665
2019 Impact of germline CTC1 alterations on telomere length in acquired bone marrow failure. British journal of haematology 15 30891747
2017 Novel biallelic missense mutations in CTC1 gene identified in a Chinese family with Coats plus syndrome. Journal of the neurological sciences 14 29111009
2023 CTC1 OB-B interaction with TPP1 terminates telomerase and prevents telomere overextension. Nucleic acids research 13 37021555
2022 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 13 35368664
2022 Pan-cancer analysis reveals that CTC1-STN1-TEN1 (CST) complex may have a key position in oncology. Cancer genetics 11 35134616
2025 CTC1-STN1-TEN1 controls DNA break repair pathway choice via DNA end resection blockade. Science (New York, N.Y.) 10 40403056
2012 Cerebroretinal microangiopathy with calcifications and cysts associated with CTC1 and NDP mutations. Journal of child neurology 10 23220793
2021 Primary Ovarian Failure in Addition to Classical Clinical Features of Coats Plus Syndrome in a Female Carrying 2 Truncating Variants of CTC1. Hormone research in paediatrics 8 34706368
2023 A novel mutation of CTC1 leads to telomere shortening in a chinese family with interstitial lung disease. Hereditas 7 37978541
2020 Ophthalmic findings and a novel CTC1 gene mutation in coats plus syndrome: a case report. Ophthalmic genetics 7 33034244
2021 miR-376a Provokes Rectum Adenocarcinoma Via CTC1 Depletion-Induced Telomere Dysfunction. Frontiers in cell and developmental biology 4 33937245
2023 Case Report: CTC1 mutations in a patient with diffuse hepatic and splenic hemangiomatosis complicated by Kasabach-Merritt syndrome. Frontiers in oncology 3 36761951
2023 Germline variant of CTC1 gene in a patient with pulmonary fibrosis and myelodysplastic syndrome. Multidisciplinary respiratory medicine 3 37404458
2025 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 2 41036624
2024 Suppression of CTC1 inhibits hepatocellular carcinoma cell growth and enhances RHPS4 cytotoxicity. Molecular biology reports 2 39001931
2016 Downregulation of SWI5 and CTC1 genes: hepatitis B virus DNA polymerase transactivated protein 1-mediated inhibition of DNA repair. Acta virologica 2 27265469
2014 Telomere stability and development of ctc1 mutants are rescued by inhibition of EJ recombination pathways in a telomerase-dependent manner. Nucleic acids research 2 25274733
2022 Transcriptomic Analysis of Conserved Telomere Maintenance Component 1 (CTC1) and Its Association with Leukemia. Journal of clinical medicine 1 36233645
2026 CTC1 mutation causing cerebro-retinal microangiopathy with calcifications and cysts type 1, masquerading as TORCH Infection. BMJ case reports 0 41554616
2026 Preimplantation genetic testing-M for pathogenic variant in CTC1 gene causing cerebroretinal microangiopathy. Journal of assisted reproduction and genetics 0 41575730
2025 STN1 Shields CTC1 From TRIM32-Mediated Ubiquitination to Prevent Cellular Aging. Aging cell 0 40923710
2024 Associations between ZNF676, CTC1 Gene Polymorphisms and Relative Leukocyte Telomere Length with Myopia and Its Degree. Biomedicines 0 38540151

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