GO:0007004 telomere maintenance via telomerase: Mechanism, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0007004 (telomere maintenance via telomerase) is the biological process that maintains proper telomeric length by the addition of telomeric repeats by the enzyme telomerase.
• Telomerase is a ribonucleoprotein reverse transcriptase that uses its own RNA template to synthesize telomeric DNA repeats, counteracting end-replication losses.
• The catalytic subunit TERT and the RNA component TERC form the core enzyme, while accessory proteins such as dyskerin (DKC1), NOP10, NHP2, GAR1, NAF1, TCAB1 and the CST complex regulate its biogenesis, trafficking and activity [1,4].
• Telomerase-dependent telomere maintenance is essential for stem cell and germline proliferation, and its reactivation is a hallmark of most cancers [1,5,7].
• Alternative lengthening of telomeres (ALT) provides a telomerase-independent mechanism in a subset of tumors, and crosstalk between telomerase and ALT pathways is an active research area.
• Experimental dissection of GO:0007004 uses CRISPR knockout, point mutation, knock-in and overexpression models combined with telomere length assays, TRAP, RNA-seq, proteomics and imaging [2,4,5,8].
Description
Telomeres are specialized nucleoprotein structures at the ends of linear chromosomes that protect genomic integrity and prevent end-to-end fusions and inappropriate DNA damage responses. Because conventional DNA polymerases cannot fully replicate chromosome ends, telomeres shorten with each cell division unless a compensatory mechanism exists. The biological process annotated as GO:0007004, telomere maintenance via telomerase, describes the maintenance of proper telomeric length by the addition of telomeric repeats by telomerase. This process is essential for the long-term proliferative capacity of stem cells, germ cells and most cancer cells, and its dysregulation is linked to aging, bone marrow failure syndromes and tumorigenesis [1,5,7]. Telomerase is a specialized ribonucleoprotein reverse transcriptase. Its catalytic subunit, telomerase reverse transcriptase (TERT), uses a template region within the telomerase RNA component (TERC) to synthesize TTAGGG repeats onto chromosome ends. The enzyme is active in early development and in adult stem compartments, but is largely silenced in most somatic cells, where telomeres progressively shorten. Reactivation of telomerase is a near-universal feature of human cancers, making GO:0007004 a central node in cancer biology and a target for therapeutic intervention [5,7]. Beyond the core TERT-TERC complex, telomerase-dependent telomere maintenance requires a network of accessory factors that control enzyme assembly, stability, trafficking to telomeres and coupling to DNA replication [1,2,4]. Recent studies have revealed that nuclear actin dynamics and DNA replication stress influence telomere maintenance by telomerase, and that disruption of factors such as ZC3H15 can entrap telomerase within Cajal bodies, compromising telomere length maintenance. These findings underscore that GO:0007004 is not a single enzymatic reaction but a regulated, multi-step cellular process.
telomere maintenance via telomerase At A Glance
| GO ID | GO:0007004 |
|---|---|
| GO term | telomere maintenance via telomerase |
| Ontology | biological_process |
| Synonym | telomerase-dependent telomere maintenance |
| Definition | The maintenance of proper telomeric length by the addition of telomeric repeats by telomerase. |
| Major function | Elongation of telomeric DNA repeats by the telomerase ribonucleoprotein to counteract replicative telomere shortening. |
| Core enzyme | Telomerase, a ribonucleoprotein reverse transcriptase composed of TERT, TERC and accessory proteins. |
| Cellular context | Nucleus, with telomerase trafficking through Cajal bodies and action at chromosome ends. |
| Related process | Alternative lengthening of telomeres (ALT), a telomerase-independent telomere maintenance mechanism. |
What Is GO:0007004?
GO:0007004, telomere maintenance via telomerase, is defined as the maintenance of proper telomeric length by the addition of telomeric repeats by telomerase. In other words, it is the telomerase-dependent branch of telomere length homeostasis, in which the telomerase ribonucleoprotein extends the 3' end of the G-rich strand of telomeric DNA using its integral RNA template, thereby compensating for the shortening that occurs during DNA replication. The synonym telomerase-dependent telomere maintenance emphasizes that this process is specifically dependent on the catalytic activity of telomerase, distinguishing it from telomerase-independent mechanisms such as ALT.
Why Is telomere maintenance via telomerase Important in Cell Biology?
GO:0007004 is important because telomerase-dependent telomere maintenance underpins the replicative potential of stem cells and germ cells, and its reactivation is a hallmark of most human cancers [1,5,7]. Loss of telomerase function causes progressive telomere shortening, which can lead to bone marrow failure and other degenerative phenotypes, whereas excessive telomerase activity supports unlimited proliferation and tumor growth [1,5]. Understanding the molecular players and regulatory steps of this process is therefore central to cancer biology, aging research and regenerative medicine, and provides a rational basis for therapeutic strategies that target telomerase or exploit telomere maintenance defects [5,6,7].
• Maintains telomere length in stem cells and germ cells, supporting tissue renewal and fertility.
• Reactivation of telomerase is a hallmark of most cancers and correlates with poor clinical outcomes in several tumor types [5,7].
• Telomerase dysfunction causes premature telomere shortening and bone marrow failure syndromes.
• Provides a therapeutic target: inhibition of hTERT/telomerase/telomere can mediate efficacy of agents such as osimertinib in EGFR-mutant lung cancer.
• Crosstalk with ALT pathway components such as POLD3 and NPM1 reveals alternative telomere maintenance vulnerabilities in osteosarcoma and other cancers.
• Nuclear actin and DNA replication stress regulate telomere maintenance by telomerase, linking cytoskeletal dynamics to genome stability.
• Telomerase reverse transcriptase can program the tumor microenvironment via regulation of the cGAS-STING pathway, extending its role beyond telomere elongation.
• Thymidine nucleotide metabolism controls human telomere length, connecting nucleotide biosynthesis to telomerase-dependent maintenance.
• Disruption of factors such as ZC3H15 compromises telomere length maintenance by entrapping telomerase within Cajal bodies, highlighting trafficking as a regulatory node.
• Pan-cancer analyses of telomere maintenance mechanisms reveal clinical relevance across tumor types.
What Happens During telomere maintenance via telomerase?
Telomerase biogenesis and assembly
In simple terms: The cell first builds the telomerase machine by assembling its RNA and protein parts.
Telomerase is a ribonucleoprotein reverse transcriptase whose core consists of the catalytic subunit TERT and the RNA component TERC, which contains the template for telomeric repeat synthesis. Assembly and maturation of the enzyme require accessory proteins including dyskerin (DKC1), NOP10, NHP2, GAR1 and NAF1, which stabilize TERC and facilitate the formation of a functional holoenzyme. TCAB1 (WRAP53) binds the CAB box of TERC and directs the enzyme to Cajal bodies, which are nuclear sites of telomerase maturation and trafficking [1,4]. Disruption of these assembly and trafficking steps, for example by loss of ZC3H15, can entrap telomerase within Cajal bodies and compromise telomere length maintenance.
Recruitment to chromosome ends
In simple terms: The finished telomerase machine must travel to the very tips of chromosomes to do its job.
Once assembled, telomerase must be recruited to telomeres, the specialized nucleoprotein structures at chromosome ends. This recruitment is coordinated with DNA replication and involves interactions with telomere-binding proteins and the replication machinery [1,2]. Nuclear actin dynamics and DNA replication stress have been shown to regulate telomere maintenance by telomerase, indicating that recruitment and action are sensitive to the state of the replication fork and the nuclear cytoskeleton. The CST complex (CTC1-STN1-TEN1) also plays a role in coordinating telomerase action with lagging-strand synthesis and in terminating telomerase extension.
Catalytic extension of telomeric DNA
In simple terms: Telomerase uses its built-in RNA template to add repeated DNA sequences onto the chromosome end.
At the telomere, TERT uses the template region of TERC to synthesize TTAGGG repeats onto the 3' end of the G-rich telomeric strand. This reverse transcription reaction is processive, allowing multiple repeats to be added in a single binding event, and is coupled to the coordinated synthesis of the complementary C-rich strand by conventional DNA polymerases. The catalytic cycle requires the telomerase RNA template, the TERT reverse transcriptase domain, and accessory factors that maintain enzyme processivity and fidelity. Thymidine nucleotide metabolism can influence this step by controlling the availability of dTTP, thereby affecting human telomere length.
Regulation by replication stress and nuclear actin
In simple terms: The cell checks whether DNA replication is proceeding normally and adjusts telomerase activity accordingly.
Telomere maintenance by telomerase is not constitutive but is regulated by cellular conditions. Nuclear actin and DNA replication stress have been identified as regulators of telomere maintenance by telomerase, linking the actin cytoskeleton and replication checkpoint to telomerase action. This regulation helps ensure that telomerase acts preferentially at telomeres that require elongation and avoids inappropriate extension that could promote genome instability. The interplay between replication stress and telomerase also has implications for cancer therapy, as replication stress-inducing agents may modulate telomerase-dependent telomere maintenance [2,5].
Coupling to cell proliferation and stemness
In simple terms: Telomerase keeps stem cells and cancer cells dividing by preserving their chromosome ends.
Telomerase-dependent telomere maintenance is tightly coupled to cell proliferation and stemness. In stem cells and germ cells, telomerase activity preserves telomere length across divisions, supporting long-term tissue renewal. In cancer cells, reactivation of telomerase is a hallmark that enables unlimited replicative potential [1,5,7]. Pan-cancer analyses of telomere maintenance mechanisms have shown that telomerase activation is clinically relevant across tumor types, and that tumors may switch between telomerase-dependent and ALT mechanisms [6,7]. Telomerase reverse transcriptase can also influence the tumor microenvironment through regulation of the cGAS-STING pathway, indicating roles beyond telomere elongation.
Key Genes Involved in GO:0007004 telomere maintenance via telomerase
The following genes and proteins are central to telomerase-dependent telomere maintenance (GO:0007004) and are frequently studied in mechanistic and translational research.
| Gene | Major Role | Research Relevance |
|---|---|---|
| TERT | Catalytic subunit of telomerase; reverse transcriptase that synthesizes telomeric repeats | Core enzyme; target for cancer therapy and stem cell engineering [1,5] |
| TERC | Telomerase RNA component; provides the template for telomeric repeat synthesis | Essential for enzyme activity; mutations cause dyskeratosis congenita |
| DKC1 | Dyskerin; stabilizes TERC and assembles the telomerase holoenzyme | Mutations cause dyskeratosis congenita and bone marrow failure |
| NOP10 | Accessory protein in telomerase holoenzyme assembly | Required for TERC stability and telomerase function |
| NHP2 | Accessory protein in telomerase holoenzyme assembly | Required for TERC stability and telomerase function |
| GAR1 | Accessory protein in telomerase holoenzyme assembly | Required for TERC stability and telomerase function |
| NAF1 | Telomerase RNA maturation factor | Required for TERC accumulation and telomerase biogenesis |
| TCAB1 (WRAP53) | Binds TERC CAB box; directs telomerase to Cajal bodies | Regulates telomerase trafficking and telomere maintenance [1,4] |
| ZC3H15 | Regulates telomerase localization; disruption entraps telomerase in Cajal bodies | Loss compromises telomere length maintenance |
| POLD3 | DNA polymerase delta subunit; involved in ALT telomere maintenance | Stabilized by NPM1 phosphorylation in ALT-positive osteosarcoma |
| NPM1 | Nucleophosmin; phosphorylation-mediated stabilization of POLD3 | Regulates ALT telomere maintenance in osteosarcoma |
| STN1 (OBFC1) | CST complex subunit; regulates telomerase action and telomere end processing | Coordinates telomerase with lagging-strand synthesis |
| CTC1 | CST complex subunit; telomere maintenance and replication | Mutations cause Coats plus syndrome |
| TEN1 | CST complex subunit; telomere protection and telomerase regulation | Regulates telomerase-dependent telomere maintenance |
| hTERT (TERT) | Human telomerase reverse transcriptase; therapeutic target | Inhibition mediates osimertinib efficacy in EGFR-mutant lung cancer |
| cGAS-STING pathway genes | Innate immune signaling regulated by telomerase reverse transcriptase | Telomerase programs the tumor microenvironment |
| Thymidine nucleotide metabolism genes | Control dTTP availability for telomeric DNA synthesis | Thymidine nucleotide metabolism controls human telomere length |
How Is telomere maintenance via telomerase Regulated?
Telomere maintenance via telomerase is regulated at multiple levels. Transcriptional control of TERT is a major determinant of telomerase activity, and TERT is silenced in most somatic cells but reactivated in cancer. Post-transcriptional regulation includes TERC maturation and stability, which depend on accessory proteins such as dyskerin, NOP10, NHP2, GAR1 and NAF1. Trafficking of the holoenzyme to Cajal bodies via TCAB1 is required for telomerase function, and disruption of this step, for example by ZC3H15 loss, impairs telomere length maintenance. Nuclear actin dynamics and DNA replication stress also regulate telomere maintenance by telomerase, linking the process to the replication checkpoint and cytoskeletal state. In addition, thymidine nucleotide metabolism controls human telomere length by influencing the availability of dTTP for telomeric DNA synthesis. Finally, telomerase reverse transcriptase can regulate the cGAS-STING pathway, indicating that telomerase activity is integrated with innate immune signaling in the tumor microenvironment.
telomere maintenance via telomerase and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| TERT | Cancer, dyskeratosis congenita, aging | CRISPR knockout and point mutation in cancer cell lines; telomere length assays [1,5] |
| TERC | Dyskeratosis congenita, bone marrow failure | Knockout and knock-in of TERC mutations in hematopoietic cells |
| DKC1 | Dyskeratosis congenita | Knockout and point mutation models in stem cells |
| POLD3 | ALT-positive osteosarcoma | Knockout and phosphorylation-site mutants in osteosarcoma lines |
| NPM1 | ALT-positive osteosarcoma | Phospho-mimetic and phospho-dead knock-in models |
Cancer
Reactivation of telomerase is a hallmark of most human cancers, enabling unlimited replicative potential [1,5,7]. Pan-cancer analyses of telomere maintenance mechanisms show that telomerase activation is clinically relevant across tumor types, and that some tumors use ALT instead [6,7]. In EGFR-mutant lung cancer, inhibition of hTERT/telomerase/telomere mediates the therapeutic efficacy of osimertinib, linking telomerase-dependent telomere maintenance to targeted therapy response. Telomerase reverse transcriptase can also program the tumor microenvironment via regulation of the cGAS-STING pathway, extending its oncogenic roles beyond telomere elongation.
Bone marrow failure and dyskeratosis congenita
Loss-of-function mutations in telomerase components, including TERT, TERC and DKC1, cause dyskeratosis congenita and related bone marrow failure syndromes characterized by premature telomere shortening. These disorders illustrate that telomerase-dependent telomere maintenance is essential for the regenerative capacity of highly proliferative tissues such as the bone marrow.
ALT-positive cancers and osteosarcoma
A subset of cancers maintain telomeres through the ALT pathway, which is independent of telomerase. In ALT-positive osteosarcoma, NPM1 phosphorylation-mediated stabilization of POLD3 supports telomere maintenance, revealing mechanisms and therapeutic opportunities distinct from telomerase inhibition. Understanding the crosstalk between telomerase-dependent and ALT mechanisms is important for designing therapies that target telomere maintenance in diverse tumor contexts [6,7].
Aging and degenerative phenotypes
Progressive telomere shortening due to insufficient telomerase activity contributes to aging phenotypes and degenerative diseases. Conversely, telomerase activation can extend replicative lifespan but may increase cancer risk, highlighting the need for precise regulation of GO:0007004 in therapeutic settings [1,5].
From telomere maintenance via telomerase-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Is TERT required for telomere maintenance in a specific cancer? | TERT knockout cell lines with telomere length and TRAP assays [1,5] |
| Does a TERC mutation impair telomerase assembly? | Point-mutation knock-in of TERC variants in stem cells |
| How does ZC3H15 loss affect telomerase localization? | ZC3H15 knockout with Cajal body imaging and telomere length assays |
| Does NPM1 phosphorylation regulate POLD3 stability in ALT? | Phospho-mimetic and phospho-dead NPM1 knock-in in osteosarcoma cells |
| Can telomerase overexpression extend replicative lifespan? | TERT overexpression in primary fibroblasts with long-term proliferation assays |
| What genes modify telomere length in a genome-wide screen? | CRISPR library screening with telomere length readouts |
How to Study the telomere maintenance via telomerase Process
| Method | What It Measures | Typical Application |
|---|---|---|
| TRF Southern blot | Terminal restriction fragment length | Telomere length in knockout and overexpression models |
| qPCR telomere length assay | Relative telomere content | High-throughput screening of telomere maintenance genes |
| TRAP assay | Telomerase enzymatic activity | Validation of TERT/TERC perturbations [1,5] |
| Telomere FISH | Telomere repeats at chromosome ends | Detection of telomere dysfunction and ALT |
| Immunofluorescence | Localization of telomerase components and Cajal bodies | Trafficking studies such as ZC3H15 loss |
| RNA-seq | Transcriptional changes upon perturbation | Pathway analysis of telomere maintenance regulators |
| Proteomics | Protein interactions and modifications | Identification of telomerase complex components |
| CRISPR library screening | Genome-wide fitness and telomere phenotypes | Discovery of novel regulators of GO:0007004 |
Telomere length measurement
Telomere length is the primary readout for GO:0007004. Techniques include terminal restriction fragment (TRF) analysis by Southern blot, quantitative PCR-based telomere length assays, and fluorescence in situ hybridization (FISH) of telomeric repeats [1,8]. These methods are used to determine whether genetic perturbations alter telomerase-dependent telomere maintenance [4,5].
Telomerase activity assays
The telomeric repeat amplification protocol (TRAP) and its quantitative variants measure telomerase enzymatic activity in cell lysates. Direct primer extension assays can measure telomerase processivity and template usage. These assays are essential for distinguishing changes in telomerase activity from changes in telomere length.
Imaging and localization
Fluorescence microscopy of telomerase components and telomere FISH can reveal trafficking and localization defects, such as entrapment of telomerase within Cajal bodies upon ZC3H15 disruption. Live-cell imaging of nuclear actin and replication stress markers can link cytoskeletal dynamics to telomere maintenance.
Genomics and proteomics
RNA-seq, proteomics and CRISPR library screening can identify regulators of telomere maintenance via telomerase. Pan-cancer genomic analyses of telomere maintenance mechanisms reveal clinically relevant subtypes and potential therapeutic targets. Proteomic approaches can detect changes in telomerase complex composition and post-translational modifications.
How CRISPR Can Be Used to Study GO:0007004 telomere maintenance via telomerase
Knockout
CRISPR knockout of TERT, TERC or accessory genes such as DKC1 and ZC3H15 is used to test requirement for telomerase-dependent telomere maintenance [1,4]. Knockout cells typically show progressive telomere shortening, reduced telomerase activity and, in cancer cells, impaired proliferation. Knockout models are also used to validate hits from CRISPR library screens.
Point Mutation
Point mutations in TERT, TERC or DKC1 can model disease-associated variants and dissect catalytic versus non-catalytic functions. For example, phospho-dead or phospho-mimetic mutations in NPM1 can test the role of phosphorylation in POLD3 stabilization and ALT telomere maintenance. Point mutation models are essential for separating telomere elongation from other telomerase functions such as cGAS-STING regulation.
Knock-in
Knock-in of tagged TERT or TERC allows visualization and purification of the telomerase complex. Knock-in of disease-relevant mutations in TERC or DKC1 can recapitulate dyskeratosis congenita phenotypes in cell models. Knock-in of phospho-mimetic NPM1 can test gain-of-function effects on ALT telomere maintenance.
Overexpression
Overexpression of TERT is used to extend replicative lifespan and to study telomerase-dependent telomere maintenance in primary cells. Overexpression models can also reveal non-telomeric functions of TERT, such as regulation of the cGAS-STING pathway and the tumor microenvironment. Controlled overexpression is valuable for testing whether increased telomerase activity is sufficient to drive telomere elongation or transformation.
How EDITGENE Supports telomere maintenance via telomerase Research
Researchers studying telomere maintenance via telomerase-related genes often need to determine whether a candidate gene is causally involved in telomere length homeostasis, telomerase activity or cancer cell proliferation. Rigorous causal testing requires precisely engineered cell models in which the gene of interest is deleted, mutated, tagged or overexpressed, combined with quantitative telomere and telomerase assays. EDITGENE provides these models and the associated screening and bioinformatics support to accelerate discovery in GO:0007004 research.
Contact EDITGENE today to design your custom CRISPR model for telomere maintenance via telomerase research.
Frequently Asked Questions About telomere maintenance via telomerase
What is GO:0007004 telomere maintenance via telomerase?
GO:0007004 is a biological process defined as the maintenance of proper telomeric length by the addition of telomeric repeats by telomerase. It is also known as telomerase-dependent telomere maintenance.
What genes are involved in telomere maintenance via telomerase?
Core genes include TERT (telomerase reverse transcriptase) and TERC (telomerase RNA component), along with accessory factors such as DKC1, NOP10, NHP2, GAR1, NAF1, TCAB1 and the CST complex components STN1, CTC1 and TEN1 [1,4].
How does telomerase maintain telomeres?
Telomerase is a ribonucleoprotein reverse transcriptase that uses the template region of TERC to synthesize TTAGGG repeats onto the 3' end of telomeric DNA, compensating for replication-associated shortening.
Why is telomerase reactivated in cancer?
Telomerase reactivation enables cancer cells to avoid replicative senescence and achieve unlimited proliferative potential, making it a hallmark of most cancers [1,5,7].
What diseases are linked to telomere maintenance via telomerase?
Dyskeratosis congenita and bone marrow failure syndromes are linked to loss-of-function mutations in telomerase components, while telomerase reactivation is linked to many cancers [1,5,7].
What is the difference between telomerase and ALT telomere maintenance?
Telomerase-dependent telomere maintenance (GO:0007004) uses the telomerase enzyme to add telomeric repeats, whereas ALT (alternative lengthening of telomeres) is a telomerase-independent mechanism that uses recombination-based processes [6,7].
How do you measure telomerase activity?
Telomerase activity is commonly measured using the TRAP assay, which detects telomeric repeat synthesis by telomerase in cell lysates [1,5].
How do you measure telomere length?
Telomere length can be measured by terminal restriction fragment (TRF) Southern blot, quantitative PCR-based assays or telomere FISH [1,8].
Can CRISPR be used to study telomere maintenance via telomerase?
Yes, CRISPR knockout, point mutation, knock-in and overexpression models are widely used to dissect the roles of TERT, TERC and accessory genes in telomere maintenance [1,4,6].
What regulates telomere maintenance via telomerase?
Regulation occurs at transcriptional, post-transcriptional and trafficking levels, and is influenced by nuclear actin dynamics, DNA replication stress and thymidine nucleotide metabolism [1,2,4,8].
Conclusion
GO:0007004, telomere maintenance via telomerase, is a fundamental biological process that preserves chromosome ends and supports the proliferative capacity of stem cells and cancer cells. The core telomerase holoenzyme, composed of TERT, TERC and accessory proteins, is regulated at multiple levels, including biogenesis, trafficking and coupling to DNA replication [1,2,4]. Dysregulation of this process contributes to cancer, bone marrow failure and aging, and crosstalk with ALT pathways adds further complexity [5,6,7]. Continued research using CRISPR-engineered cell models and quantitative telomere assays will refine our understanding of GO:0007004 and inform therapeutic strategies targeting telomere maintenance.
References
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- 2. Harman A et al.. 2025. Nuclear actin and DNA replication stress regulate telomere maintenance by telomerase.. Nat Commun 16(1):10193 PMID: 41331243
- 3. Akincilar SC et al.. 2025. Evolutionarily conserved role of telomerase reverse transcriptase in programming the microenvironment via regulation of the cGAS-STING pathway.. Nat Cell Biol 27(8):1342-1356 PMID: 40770487
- 4. Wang C et al.. 2025. Disruption of ZC3H15 compromises telomere length maintenance by entrapping telomerase within cajal bodies.. Cell Biosci 15(1):107 PMID: 40696438
- 5. Chen Z et al.. 2024. Inhibition of hTERT/telomerase/telomere mediates therapeutic efficacy of osimertinib in EGFR mutant lung cancer.. J Exp Med 221(11) PMID: 39297884
- 6. Zhao R et al.. 2026. NPM1 phosphorylation-mediated telomere maintenance via stabilization of POLD3 in ALT-positive osteosarcoma: unraveling mechanisms and therapeutic opportunities.. Theranostics 16(8):4224-4244 PMID: 41695477
- 7. Sung JY et al.. 2021. Pan-Cancer Analysis of Clinical Relevance via Telomere Maintenance Mechanism.. Int J Mol Sci 22(20) PMID: 34681758
- 8. Mannherz W et al.. 2023. Thymidine nucleotide metabolism controls human telomere length.. Nat Genet 55(4):568-580 PMID: 36959362
