Relevant bibliographies by topics / Telomere

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Academic literature on the topic 'Telomere'

Author: Grafiati
Published: 4 June 2021
Last updated: 30 July 2024

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Journal articles on the topic "Telomere"

1

Lin, Chi-Ying, Hsih-Hsuan Chang, Kou-Juey Wu, Shun-Fu Tseng, Chuan-Chuan Lin, Chao-Po Lin, and Shu-Chun Teng. "Extrachromosomal Telomeric Circles Contribute to Rad52-, Rad50-, and Polymerase δ-Mediated Telomere-Telomere Recombination in Saccharomyces cerevisiae." Eukaryotic Cell 4, no. 2 (February 2005): 327–36. http://dx.doi.org/10.1128/ec.4.2.327-336.2005.

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ABSTRACT Telomere maintenance is required for chromosome stability, and telomeres are typically replicated by the telomerase reverse transcriptase. In both tumor and yeast cells that lack telomerase, telomeres are maintained by an alternative recombination mechanism. By using an in vivo inducible Cre-loxP system to generate and trace the fate of marked telomeric DNA-containing rings, the efficiency of telomere-telomere recombination can be determined quantitatively. We show that the telomeric loci are the primary sites at which a marked telomeric ring-containing DNA is observed among wild-type and surviving cells lacking telomerase. Marked telomeric DNAs can be transferred to telomeres and form tandem arrays through Rad52-, Rad50-, and polymerase δ-mediated recombination. Moreover, increases of extrachromosomal telomeric and Y′ rings were observed in telomerase-deficient cells. These results imply that telomeres can use looped-out telomeric rings to promote telomere-telomere recombination in telomerase-deficient Saccharomyces cerevisiae.
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Brault, Marie Eve, and Chantal Autexier. "Telomeric recombination induced by dysfunctional telomeres." Molecular Biology of the Cell 22, no. 2 (January 15, 2011): 179–88. http://dx.doi.org/10.1091/mbc.e10-02-0173.

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Telomere maintenance is essential for cellular immortality, and most cancer cells maintain their telomeres through the enzyme telomerase. Telomeres and telomerase represent promising anticancer targets. However, 15% of cancer cells maintain their telomeres through alternative recombination-based mechanisms, and previous analyses showed that recombination-based telomere maintenance can be activated after telomerase inhibition. We determined whether telomeric recombination can also be promoted by telomere dysfunction. We report for the first time that telomeric recombination can be induced in human telomerase-positive cancer cells with dysfunctional telomeres.
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Kishtagari, Ashwin, and Justin Watts. "Biological and clinical implications of telomere dysfunction in myeloid malignancies." Therapeutic Advances in Hematology 8, no. 11 (October 6, 2017): 317–26. http://dx.doi.org/10.1177/2040620717731549.

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Telomeres at the ends of linear chromosomes protect the genome. Telomeres shorten with each round of cell division, placing a finite limit on cell growth. Telomere attrition is associated with cell senescence and apoptosis. Telomerase, a specialized ribonucleoprotein complex, maintains telomeres homeostasis through repeat addition of telomere sequences to the 3′ telomeric overhang. Telomere biology is closely related to cancer and normal aging. Upregulation of telomerase or activation of the alternative pathway of telomere lengthening is a hallmark of cancer cells, making telomerase an attractive target for cancer therapeutics. In this review, we will discuss telomere biology and the prognostic implications of telomere length in acute myeloid leukemia, and review exciting new investigational approaches using telomerase inhibitors in acute myeloid leukemia and other myeloid malignancies.
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Bechard, Laura H., Bilge D. Butuner, George J. Peterson, Will McRae, Zeki Topcu, and Michael J. McEachern. "Mutant Telomeric Repeats in Yeast Can Disrupt the Negative Regulation of Recombination-Mediated Telomere Maintenance and Create an Alternative Lengthening of Telomeres-Like Phenotype." Molecular and Cellular Biology 29, no. 3 (November 24, 2008): 626–39. http://dx.doi.org/10.1128/mcb.00423-08.

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ABSTRACT Some human cancers maintain telomeres using alternative lengthening of telomeres (ALT), a process thought to be due to recombination. In Kluyveromyces lactis mutants lacking telomerase, recombinational telomere elongation (RTE) is induced at short telomeres but is suppressed once telomeres are moderately elongated by RTE. Recent work has shown that certain telomere capping defects can trigger a different type of RTE that results in much more extensive telomere elongation that is reminiscent of human ALT cells. In this study, we generated telomeres composed of either of two types of mutant telomeric repeats, Acc and SnaB, that each alter the binding site for the telomeric protein Rap1. We show here that arrays of both types of mutant repeats present basally on a telomere were defective in negatively regulating telomere length in the presence of telomerase. Similarly, when each type of mutant repeat was spread to all chromosome ends in cells lacking telomerase, they led to the formation of telomeres produced by RTE that were much longer than those seen in cells with only wild-type telomeric repeats. The Acc repeats produced the more severe defect in both types of telomere maintenance, consistent with their more severe Rap1 binding defect. Curiously, although telomerase deletion mutants with telomeres composed of Acc repeats invariably showed extreme telomere elongation, they often also initially showed persistent very short telomeres with few or no Acc repeats. We suggest that these result from futile cycles of recombinational elongation and truncation of the Acc repeats from the telomeres. The presence of extensive 3′ overhangs at mutant telomeres suggests that Rap1 may normally be involved in controlling 5′ end degradation.
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Smogorzewska, Agata, Bas van Steensel, Alessandro Bianchi, Stefan Oelmann, Matthias R. Schaefer, Gisela Schnapp, and Titia de Lange. "Control of Human Telomere Length by TRF1 and TRF2." Molecular and Cellular Biology 20, no. 5 (March 1, 2000): 1659–68. http://dx.doi.org/10.1128/mcb.20.5.1659-1668.2000.

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ABSTRACT Telomere length in human cells is controlled by a homeostasis mechanism that involves telomerase and the negative regulator of telomere length, TRF1 (TTAGGG repeat binding factor 1). Here we report that TRF2, a TRF1-related protein previously implicated in protection of chromosome ends, is a second negative regulator of telomere length. Overexpression of TRF2 results in the progressive shortening of telomere length, similar to the phenotype observed with TRF1. However, while induction of TRF1 could be maintained over more than 300 population doublings and resulted in stable, short telomeres, the expression of exogenous TRF2 was extinguished and the telomeres eventually regained their original length. Consistent with their role in measuring telomere length, indirect immunofluorescence indicated that both TRF1 and TRF2 bind to duplex telomeric DNA in vivo and are more abundant on telomeres with long TTAGGG repeat tracts. Neither TRF1 nor TRF2 affected the expression level of telomerase. Furthermore, the presence of TRF1 or TRF2 on a short linear telomerase substrate did not inhibit the enzymatic activity of telomerase in vitro. These findings are consistent with the recently proposed t loop model of telomere length homeostasis in which telomerase-dependent telomere elongation is blocked by sequestration of the 3′ telomere terminus in TRF1- and TRF2-induced telomeric loops.
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Martin, Aegina Adams, Isabelle Dionne, Raymund J. Wellinger, and Connie Holm. "The Function of DNA Polymerase α at Telomeric G Tails Is Important for Telomere Homeostasis." Molecular and Cellular Biology 20, no. 3 (February 1, 2000): 786–96. http://dx.doi.org/10.1128/mcb.20.3.786-796.2000.

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ABSTRACT Telomere length control is influenced by several factors, including telomerase, the components of telomeric chromatin structure, and the conventional replication machinery. Although known components of the replication machinery can influence telomere length equilibrium, little is known about why mutations in certain replication proteins cause dramatic telomere lengthening. To investigate the cause of telomere elongation in cdc17/pol1 (DNA polymerase α) mutants, we examined telomeric chromatin, as measured by its ability to repress transcription on telomere-proximal genes, and telomeric DNA end structures in pol1-17 mutants. pol1-17 mutants with elongated telomeres show a dramatic loss of the repression of telomere-proximal genes, or telomeric silencing. In addition,cdc17/pol1 mutants grown under telomere-elongating conditions exhibit significant increases in single-stranded character in telomeric DNA but not at internal sequences. The single strandedness is manifested as a terminal extension of the G-rich strand (G tails) that can occur independently of telomerase, suggesting thatcdc17/pol1 mutants exhibit defects in telomeric lagging-strand synthesis. Interestingly, the loss of telomeric silencing and the increase in the sizes of the G tails at the telomeres temporally coincide and occur before any detectable telomere lengthening is observed. Moreover, the G tails observed incdc17/pol1 mutants incubated at the semipermissive temperature appear only when the cells pass through S phase and are processed by the time cells reach G1. These results suggest that lagging-strand synthesis is coordinated with telomerase-mediated telomere maintenance to ensure proper telomere length control.
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Kondratieva, Yu A., and L. P. Mendeleeva. "Characteristics of telomere length in patients with hematological diseases (literature review)." Oncohematology 16, no. 1 (April 14, 2021): 23–30. http://dx.doi.org/10.17650/1818-8346-2021-16-1-23-30.

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Telomeres are protein structures that regulate the process of cellular aging and play the role of a protective “cap” on the end sections of chromosomes. The telomeres of nucleated cells undergo permanent shortening during their lifetime as a result of multiple cycles of DNA replication. The enzyme that provides completion of the missing telomeric repeats at the ends of chromosomes is called “telomerase”. However, recovery of critically short telomeres by telomerase or recombination in somatic cells is limited due to the presence of a large accumulation of unclosed telomeres, which triggers apoptosis. The death of stem cells due to telomere depletion ensures the selection of abnormal cells in which the genome instability contributes to malignant progression. During carcinogenesis, cells acquire mechanisms for maintaining telomeres in order to avoid programmed death. In addition, tumor cells are able to support the telomere's DNA, counteracting its shortening and premature death. Activation of telomere length maintenance mechanisms is a hallmark of most types of cancers. In the modern world, there is an increasing interest in studying the biological characteristics of telomeres. The development of new methods for measuring telomere length has provided numerous studies to understand the relationship between telomere length of human nucleated cells and cancer. Perhaps maintaining telomere length will be an important step, determining the course and prognosis of the disease. The purpose of this review is to provide an analysis of published data of the role and significance of telomere length in patients with hematological malignancies.
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Perera, Omesha N., Alexander P. Sobinoff, Erdahl T. Teber, Ashley Harman, Michelle F. Maritz, Sile F. Yang, Hilda A. Pickett, et al. "Telomerase promotes formation of a telomere protective complex in cancer cells." Science Advances 5, no. 10 (October 2019): eaav4409. http://dx.doi.org/10.1126/sciadv.aav4409.

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Telomerase is a ribonucleoprotein complex that catalyzes addition of telomeric DNA repeats to maintain telomeres in replicating cells. Here, we demonstrate that the telomerase protein hTERT performs an additional role at telomeres that is independent of telomerase catalytic activity yet essential for telomere integrity and cell proliferation. Short-term depletion of endogenous hTERT reduced the levels of heat shock protein 70 (Hsp70-1) and the telomere protective protein Apollo at telomeres, and induced telomere deprotection and cell cycle arrest, in the absence of telomere shortening. Short-term expression of hTERT promoted colocalization of Hsp70-1 with telomeres and Apollo and reduced numbers of deprotected telomeres, in a manner independent of telomerase catalytic activity. These data reveal a previously unidentified noncanonical function of hTERT that promotes formation of a telomere protective complex containing Hsp70-1 and Apollo and is essential for sustained proliferation of telomerase-positive cancer cells, likely contributing to the known cancer-promoting effects of both hTERT and Hsp70-1.
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Fernandes, Stina George, Rebecca Dsouza, Gouri Pandya, Anuradha Kirtonia, Vinay Tergaonkar, Sook Y. Lee, Manoj Garg, and Ekta Khattar. "Role of Telomeres and Telomeric Proteins in Human Malignancies and Their Therapeutic Potential." Cancers 12, no. 7 (July 14, 2020): 1901. http://dx.doi.org/10.3390/cancers12071901.

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Telomeres are the ends of linear chromosomes comprised of repetitive nucleotide sequences in humans. Telomeres preserve chromosomal stability and genomic integrity. Telomere length shortens with every cell division in somatic cells, eventually resulting in replicative senescence once telomere length becomes critically short. Telomere shortening can be overcome by telomerase enzyme activity that is undetectable in somatic cells, while being active in germline cells, stem cells, and immune cells. Telomeres are bound by a shelterin complex that regulates telomere lengthening as well as protects them from being identified as DNA damage sites. Telomeres are transcribed by RNA polymerase II, and generate a long noncoding RNA called telomeric repeat-containing RNA (TERRA), which plays a key role in regulating subtelomeric gene expression. Replicative immortality and genome instability are hallmarks of cancer and to attain them cancer cells exploit telomere maintenance and telomere protection mechanisms. Thus, understanding the role of telomeres and their associated proteins in cancer initiation, progression and treatment is very important. The present review highlights the critical role of various telomeric components with recently established functions in cancer. Further, current strategies to target various telomeric components including human telomerase reverse transcriptase (hTERT) as a therapeutic approach in human malignancies are discussed.
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Henderson, S., R. Allsopp, D. Spector, S. S. Wang, and C. Harley. "In situ analysis of changes in telomere size during replicative aging and cell transformation." Journal of Cell Biology 134, no. 1 (July 1, 1996): 1–12. http://dx.doi.org/10.1083/jcb.134.1.1.

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Telomeres have been shown to gradually shorten during replicative aging in human somatic cells by Southern analysis. This study examines telomere shortening at the single cell level by fluorescence in situ hybridization (FISH). FISH and confocal microscopy of interphase human diploid fibroblasts (HDFs) demonstrate that telomeres are distributed throughout the nucleus with an interchromosomal heterogeneity in size. Analysis of HDFs at increasing population doubling levels shows a gradual increase in spot size, intensity, and detectability of telomeric signal. FISH of metaphase chromosomes prepared from young and old HDFs shows a heterogeneity in detection frequency for telomeres on chromosomes 1, 9, 15, and Y. The interchromosomal distribution of detection frequencies was similar for cells at early and late passage. The telomeric detection frequency for metaphase chromosomes also decreased with age. These observations suggest that telomeres shorten at similar rates in normal human somatic cels. T-antigen transformed HDFs near crisis contained telomere signals that were low compared to nontransformed HDFs. A large intracellular heterogeneity in telomere lengths was detected in two telomerase-negative cell lines compared to normal somatic cells and the telomerase-positive 293 cell line. Many telomerase-negative immortal cells had telomeric signals stronger than those in young HDFs, suggesting a different mechanism for telomere length regulation in telomerase-negative immortal cells. These studies provide an in situ demonstration of interchromosomal heterogeneity in telomere lengths. Furthermore, FISH is a reliable and sensitive method for detecting changes in telomere size at the single cell level.
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Dissertations / Theses on the topic "Telomere"

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Johnston, Jeffrey Scott. "Combination therapy targeting telomere and telomerase /." The Ohio State University, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=osu1486462067841929.

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Hirsch, Erica. "Telomerase activity and telomere lengths in fibroblast cells treated with ependymin peptide mimetics." Link to electronic thesis, 2005. http://www.wpi.edu/Pubs/ETD/Available/etd-050505-134911/.

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Shakirov, Yevgeniy Vitalievich. "Telomeres and telomere binding proteins in Arabidopsis thaliana." Diss., Texas A&M University, 2004. http://hdl.handle.net/1969.1/422.

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Telomeres are important protein-DNA structures at the ends of linear eukaryotic chromosomes that are necessary to prevent chromosome fusions and exonuclease attack. We found that telomere tracts in Arabidopsis are fairly uniformly distributed throughout a size range of 2-9kb. Unexpectedly, telomeres in WS plants displayed a bimodal size distribution with some individuals exhibiting 4-8 kb telomeres and others 2-5 kb telomeres. We also examined the dynamics of telomere tracts on individual chromosome ends. Following the fate of telomeres in plants through successive generations, we found that the shortest telomeres were typically elongated in the subsequent generation, while the longest telomeres were usually shortened. Thus, telomere length homoeostasis is achieved through intermittent telomerase action on shorter telomeres to attain an optimal size.Single-strand telomere binding proteins were also analyzed. Four major telomere binding protein complexes from cauliflower were identified and their DNA-binding properties characterized. The DNA-binding component of one of the complexes was purified and analyzed by mass-spectrometry. Peptide mass data was used to search for putative protein candidates from the Arabidopsis thaliana database. Additionally, two Arabidopsis genes, AtPot1 and AtPot2, were identified and characterized. The genes encode two single-strand telomeric DNA binding proteins. AtPot1 and AtPot2 proteins can homo- and heterodimerize in vitro. Pot1 protein predominantly localizes to the nucleolus, whereas Pot2 is exclusively nuclear. Plants over-expressing full-length Pot1 and Pot2 proteins had no obvious phenotype, while over-expression of P2DBD and P1∆DBD caused moderate telomere shortening. Plants over-expressing P2DBD had severe morphological and reproductive defects, multiple chromosome abnormalities and aneuploidy. Over-expression of a chimeric protein DBD-P1∆DBD led to rapid telomere shortening, confirming the involvement of Arabidopsis Pot proteins in telomere length maintenance. Intriguingly, telomerase in DBD-P1∆DBD-EYFP plants is inactivated, suggesting that Pot proteins are also involved in regulation of telomerase activity. The analysis of Arabidopsis telomeres and telomere binding proteins will provide additional information towards understanding the role of the telomeric nucleoprotein complex in eukaryotic chromosome biology.
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Östlund-Lagerström, Lina. "Effect of long-term ultra-endurance training on telomere length and telomere regulatory protein expressions in vastus lateralis of healthy humans." Thesis, Örebro universitet, Hälsoakademin, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-15859.

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Gonzàlez, Busqué Núria 1980. "Snail1 controls telomere integrity and transcription and telomerase expression." Doctoral thesis, Universitat Pompeu Fabra, 2017. http://hdl.handle.net/10803/663193.

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Snail1 transcription factor is the key inducer of epithelial-to-mesenchymal transition (EMT). Here, we describe a novel role for Snail1 on the regulation of telomere integrity and transcription as well as telomerase expression. FISH assays indicate an increase of telomere alterations in Snail1-depleted mouse mesenchymal stem cells (MSCs) and shorter telomeres. However, these cells present higher levels of TERT since Snail1 represses its expression, meaning that other mechanisms in telomere homeostasis are involved. In fact, telomeres are transcribed into a long non-coding RNA called telomeric repeat-containing RNA (TERRA). Here we report that Snail1 regulates TERRA transcription by repressing TERRA 2q, 11q and 18q. TERRA and TERT are transiently down-regulated during EMT in NMuMG cells. Ectopic expression of TERRA affects the transcription of some genes induced during EMT such as fibronectin whereas TERT does not modify those genes. We propose that Snail1 control of TERRA besides being required for telomere maintenance is also necessary for the expression of a subset of mesenchymal genes.
El factor de transcripció Snail1 és el principal inductor de la transició epiteli mesènquima (EMT). Aquí describim un nou paper de Snail1 en la regulació de la integritat i transcripció telomèrica i també en l’expressió de la telomerasa. El FISH mostra un augment de les alteracions telomèriques en les MSCs deficients per Snail1 així com telòmers més curts. Malgrat això, aquestes cèl·lules presenten nivells més alts de telomerasa degut a que Snail1 en reprimeix la seva expressió, la qual cosa significa que hi ha altres mecanismes involucrats en l’homeòstasi telomèrica. De fet, els telòmers es transcriuen en uns llargs RNA no codificants anomenats TERRA. Aquí mostrem que Snail1 regula la transcripció de TERRA reprimint TERRA 2q, 11q I 18q. L’expressió de TERRA i TERT disminueix de forma transitòria durant l’EMT en les cèl·lules NMuMG. L’expressió ectòpica de TERRA afecta la transcripció d’alguns gens induïts durant l’EMT com la fibronectina, mentres que TERT no modifica aquests gens. Proposem que el control de TERRA per part de Snail1 no només és necessari pel manteniment telomèric sinó també per l’expressió d’un subconjunt de gens mesenquimals.
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Drummond, Mark William. "Telomere dynamics and telomerase expression in chronic myeloid leukaemia." Thesis, University of Glasgow, 2003. http://theses.gla.ac.uk/41113/.

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INTRODUCTION: Chronic myeloid leukaemia (CML) is a clonal myeloproliferative disorder of the haemopoietic stem cell (HSC), with a variable clinical course. Chronic phase (CP) disease, typically of 4-5 years duration, progresses to accelerated (AP) and then blastic phase (BP), with the latter behaving as a particularly aggressive acute leukaemia of either myeloid (MBP) or lymphoid (LBP) lineage. Treatment is most successful when delivered in CP, and accurate prognostic indices are required to individualise treatment. Increased telomere shortening has been described during progression of CML, and may be of prognostic relevance. Paradoxically, telomerase activity (TA, as determined by the TRAP assay) has been shown to be elevated in the CP stem/progenitor cell (CD34+) compartment: however this may not accurately reflect telomere maintenance in-vivo. We sought to further define the prognostic significance of telomere shortening at diagnosis of CML, monitor the rate of telomere loss during the disease and characterise expression of the major telomerase components (hTR and hTERT) in CD34+ selected cells at diagnosis and during disease progression. METHODS: Peripheral blood leucocyte (PBL) telomere length measurement was performed by flow-FISH on cohorts of normal individuals, patients at diagnosis and all stages of CML. To define the degree of telomere shortening in individual patients at diagnosis ex-vivo expanded (BCR-ABL') T-cells were used as an internal control for 'normal' somatic cell telomere length. Expression of hTERT and hTR was quantified by Q RT-PCR and hTERT mRNA splice variants detected by RT-PCR. CD34+ selected cells from CML patients were confirmed as BCR-ABL+ by FISH. TA was determined by TRAP assay. RESULTS: Telomere shortening in CP and AP CIVIL patients progressed at 10-20 times the rate of age-related shortening observed in the normal control group. Furthermore, high-risk prognostic score patients at diagnosis had significantly shorter telomeres than low-risk patients. High purity CD34+ selected cells from CML, as compared to normal, demonstrated increased TRAP activity which correlated with the proportion of cycling cells. However, hTERT mRNA expression was not significantly elevated. Unexpectedly, Q-RT-PCR for hTR demonstrated a mean five-fold reduction in levels in the CML samples, raising the possibility that telomere homeostasis is disrupted in CML. In BP samples, hTERT expression was significantly lower in MBP than LBP and this was mirrored by a corresponding shift in hTERT splicing patterns. MBP hTERT expression correlated inversely with telomere length. CONCLUSIONS; In summary, increased TRAP activity is not synonymous with telomere maintenance in CML, and dysregulated expression of hTR may contribute to the telomere loss observed in these patients. Indeed TRAP activity appeared largely dependent on the proportion of cycling cells. In the context of progressive (i.e. BP) disease, hTERT expression is lineage and telomere length dependent, thus explaining inconsistent reports of TA levels in BP samples. We have also demonstrated that subtle shifts in splicing of hTERT mRNA is likely to have a regulatory role in primary HSC. In prognostic terms telomere shortening in CML is greatest in high-risk score patients at diagnosis, and occurs rapidly during disease progression. These data further emphasise the potential clinical utility of telomere length measurement for prognostic modelling and monitoring of disease progression.
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Karpov, Victor. "A study on telomere protection and telomerase-and-cap-independent mechanisms of telomere maintenance in yeast Saccharomyces cerevisiae." Mémoire, Université de Sherbrooke, 2008. http://savoirs.usherbrooke.ca/handle/11143/3940.

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An SGA approach to discover cdc13-1ts supressors. Telomeres, the DNA-protein complexes at the end of eukaryotic chromosomes, are essential for chromosomal stability. In yeast, the telomeric single-strand binding protein Cdc13p has multiple important roles related to telomere maintenance: (1) telomeric"capping"--protection of telomeres by forming complexes with yKu70/80 and with Stn1p/Ten1p; (2) positive regulation of telomere replication via interaction with Est1p, which is a part of telomerase; (3) negative regulation of telomerase by the recruitment of telomere elongation suppressors Stn1p and Ten1p. In an attempt to identify genes that are involved in the deleterious outcome of an absence of Cdc13p, we screened the yeast gene knock-out library for genes that could suppress the growth defect of cdc13-1 cells at 33ê C. For this purpose, we performed an SGA array experiment. We scored for the ability of double mutant haploids to grow at 33ê C. Eventually, we hoped to find the elusive genes involved in telomere 5'-end processing (exonucleases). Based on the comparative analysis of growth properties of the strains (23ê C vs 33ê C), the initial screen identified up to 111 genes that displayed an apparent growth at 33ê C. In order to verify these results, diploids were regenerated, sporulated, microdissected, and haploid double mutants cdc13-1 yfg[deletion] were isolated from 38 potential cdc13-1 suppressors. Unfortunately, this verification failed to reproduce a suppression of the growth defect by any of the selected genes at any temperature. While disappointing, the results reemphasize that careful re-examination of large scale SGA approaches are indispensable before going on to more involved experimentation. Similarities and differences between adaptation to DNA double-strand break and to telomere uncapping in yeast Saccharomyces cerevisiae. It was previously shown that a certain proportion of telomerase negative survivor cells (both type I and type II cells) is able to survive in the absence of the telomere capping protein Cdc13p. These strains (named [deletion]13s) were characterized in great detail and one of their discovered features was a striking ability to continuously inactivate DNA-damage checkpoints. Based on structural similarities between DNA double strand breaks (DSB) and unprotected telomeres, we attempted to verify if the molecular mechanisms regulating adaptation to a single irreparable DSB also regulate adaptation to a loss of Cdc13p. For this purpose we created three tlc1[deletion] cdc13[deletion] strains also harboring DSB adaptation related mutations tid1[deletion], ptc2[deletion] and rfa1-t11. After deprotection of their telomeres, mutant survivor cells showed similar cell cycle progression patterns as compared to the cells where a single irreparable DSB was introduced. Adaptation defective mutants tid1[deletion] and ptc2[deletion] demonstrated an inability to adapt to telomere uncapping and to resume cell cycle. Interestingly, cells harboring the rfa1-t11 allele, which was reported to suppress adaptation defects of other mutations, did not show any distinguishable phenotype in terms of initial adaptation to telomere deprotection; i.e. rfa1-t11 mutant survivors do escape the G2/M arrest and re-enter the cell cycle. However, all three mutant survivor strains failed to produce viable [deletion]13 capping independent cells, which is consistent with the hypothesis that adaptation to loss of Cdc13p depends on the same pathway as the previously reported adaptation phenomenon. Finally, we report the surprising finding that if cells had once experienced an adapted [deletion]13 state, they will re-produce capping negative survivors much more readily. Thus, while a culture of type II survivor cells generates [deletion]13s at a rate of about 1×10 -5 events per division, cells that had been [deletion]13s and re-transformed with a Cdc13p carrying plasmid will produce capping independent cells at about 1×10-2 events per division. We are currently examining why these cells re-generate [deletion]13 cell lines more readily and suspect structural differences in telomere terminal sequence arrangements.
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Fakhoury, Johans. "Conserved and divergent mouse and human telomerase and telomere regulation: implications for the development and validation of telomerase and telomere-specific anticancer strategies." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=94905.

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Telomerase synthesizes telomeric sequences and is minimally composed of a reverse transcriptase (RT) (TERT) and RNA (TR). We reconstituted heterologous mouse and human TERT-TR and chimeric mTERT-hTERT-hTR complexes in vitro and in immortalized human alternative lengthening of telomere (ALT) cells. Our data suggest that species-specific determinants of activity, processivity, and telomere function map not only to TR, but also to the TERT component. hTERT-hTR, but not heterologous TERT-TR complexes, nor chimeric mTERT-hTERT-hTR complexes, significantly reduced the percentage of chromosomes without telomeric signals in ALT cells. Moreover, heterologous and chimeric complexes were defective in recruitment to telomeres. Our results suggest a requirement for several hTERT domains and interaction with multiple proteins for proper recruitment of telomerase to the shortest telomeres in human ALT cells. The ability of hTERT to elongate short mouse telomeres, and the inability of mTERT to elongate short human telomeres suggest that mechanisms regulating recruitment and activity of hTERT at short telomeres may be less stringently regulated than mechanisms regulating mTERT recruitment and activity at short telomeres. Results such as these may lead to the design of better strategies for inhibiting telomerase and validation using rodent models. For example, TERT domains that confer similar functions in human and mouse cells may be better targets than domains with species-restricted functions. We also tested the specificity of a novel class of platinum(II) G-quadruplex stabilizers at inhibiting telomerase activity. We showed that these ligands efficiently stabilize telomeres and inhibit telomerase activity with comparable potency to telomestatin (a potent telomerase inhibitor). Additionally, these ligands may present a potent dual action strategy to not only inhibit telomerase function, but also disrupt telomere function and assembly. Accordingly, targeting telomere function
La télomérase synthétise les séquences télomériques et se compose minimalement d'une sous-unité transcriptase inverse (TERT) et d'un fragment d'ARN (TR). Nous avons reconstitué des complexes hétérologues TERT-TR humains et murins ainsi que des complexes chimériques mTERT-hTERT-hTR in vitro et dans des cellules immortalisées utilisant un mécanisme alternatif d'élongation des télomères (cellules ALT). Nos résultats suggèrent que les déterminants espèce-spécifiques de l'activité, la processivité et la fonction télomérique sont attribués non seulement au composant TR mais aussi au composant TERT de la télomérase. Les complexes hTERT-hTR, mais non les complexes hétérologues TERT-TR ou mTERT-hTERT-hTR ont diminué le pourcentage de chromosomes sans signal télomérique de façon significative lorsqu'exprimés dans des cellules ALT. De plus, il a été démontré que les complexes hétérologues et chimériques sont déficients quant à leur recrutement aux télomères. Nos résultats suggèrent que plusieurs domaines de TERT et la présence d'interactions entre plusieurs protéines sont requis pour le recrutement de la télomérase aux télomères les plus courts dans les cellules ALT. La capacité de hTERT à allonger les télomères murins les plus courts, et l'incapacité de mTERT à allonger les télomères humains les plus courts suggèrent que les mécanismes régulant le recrutement et l'activité de hTERT aux télomères les plus courts seraient régulés de façon moins rigoureuse que les mécanismes régulant ceux de mTERT. De tels résultats pourraient mener à la création de meilleures stratégies visant à inhiber la télomérase et la validation de celles-ci dans des modèles murins. Par exemple, les domaines de TERT qui confèrent des fonctions similaires dans les cellules humaines et murines risquent de représenter de meilleurs cibles thérapeutiques que les domaines de TERT possédant des fonctions espèce-spécifiques.$
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Choi, Eugene Ho Yan. "Investigating spontaneous activation of two telomere maintenance mechanisms in the same cancer cells." Thesis, The University of Sydney, 2019. http://hdl.handle.net/2123/20766.

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Telomeres are biological constructs that protect the genomic information from DNA damage repair pathways and chromosomal fusions. Telomeres shorten every cell division and when the telomeres become critically short the cells become senescent. Cancer cells overcome this hindrance and proliferate infinitely via the activation of a telomere maintenance mechanism (TMM). Current literature suggests most cancers maintain their telomeres via two known mechanisms. The first involves telomerase, a ribonucleoprotein, and the other TMM, Alternative Lengthening of Telomeres (ALT), is independent of this ribonucleoprotein. Normal somatic cells do not utilise a TMM, TMMs are ideal targets for the generation of selective anti-cancer therapeutics. There is a widespread assumption in this field of research that ALT and telomerase are mutually exclusive. A prior study in the Reddel laboratory investigated the possibility that spontaneous activation of both TMMs within a single cell can occur. A melanoma cell line, LOX IMVI, was characterised to have telomerase activity in addition to the phenotypic characteristics of ALT. To identify whether both TMMs actually contributed to telomere length maintenance in LOX IMVI cells, telomerase activity was abrogated. My main contribution to this study was to examine telomere lengths in these telomerase-null cells over the course of 200 population doublings. Telomere lengths continued to decrease throughout that entire time. Therefore, no evidence was obtained that ALT contributes to telomere length maintenance in LOX IMVI cells. I then found that another human cell line, 1301, which is derived from a paediatric acute lymphoblastoid leukaemia, has telomerase activity and features of ALT activity in every subclone. To determine whether ALT and telomerase are contributing to telomere length maintenance in these cells, I used CRISPR/Cas9 to knock out the TERC gene, which encodes the RNA subunit of telomerase. Knockout was confirmed in eight subclones and were passaged long-term with seven controls. In seven of the treated clones telomere length declined detectably, but in one clone there was a negligible rate of decline. To my knowledge, this is the first evidence indicating that functional levels of telomerase and ALT activity may be spontaneously activated in the same cancer cells.
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Dagg, Rebecca Ann. "The extensive proliferation of human cancer cells with ever-shorter telomeres." Thesis, The University of Sydney, 2017. http://hdl.handle.net/2123/17341.

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Cellular immortalisation is currently regarded as an essential step in malignant transformation and is consequently considered a hallmark of cancer. Acquisition of replicative immortality is achieved by activation of a telomere lengthening mechanism (TLM), either telomerase or the alternative lengthening of telomeres (ALT), to counter normal telomere attrition. However, a proportion of malignancies are reported to be TLM-negative. The lack of serial untreated malignant human tumour samples over time has made it impossible to examine telomere length over time and hence determine whether they are truly TLM-deficient, or whether this is the result of false-negative assays. Here we describe a subset (11%) of high-risk neuroblastomas (NB) that lack evidence of any significant TLM activity despite a 51% 5-year mortality rate. Two NB cell lines derived from such tumours proliferated for 500 population doublings (PDs) with ever-shorter telomeres (EST). The EST cells had exceptionally long and heterogeneous telomere lengths as measured by terminal restriction fragment analysis and telomere fluorescence in situ hybridisation. Both cell lines were telomerase negative during culturing and did not have elevated markers of ALT or associated gene mutations. The telomeres of these cells shortened by 80 and 55 bases/PD, consistent with telomere attrition due to normal cell division, but did not reach senescence after 500 PDs in culture. This is conclusive evidence that cells from highly malignant, lethal tumours are able to undergo continuous proliferation in spite of an EST phenotype. The EST phenotype was rescued by activation of telomerase (via transduction with hTERT expression constructs) or ALT (spontaneous occurrence of a nonsense TP53 mutation, followed by spontaneous activation of ALT after 100 PDs). We also found that NB EST cells are very sensitive to topoisomerase I inhibitors indicating the potential to target the EST phenotype with topoisomerase I inhibitors in high-risk NB.
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Books on the topic "Telomere"

1

Lingner, Joachim, Dorothy Shippen, and Vicki Lundblad. Abstracts of papers presented at the 2007 meeting on telomeres & telomerase: May 2-May 6, 2007. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory, 2007.

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Lundblad, Victoria. Abstracts of papers presented at the 2005 meeting on telomeres & telomerase, May 4-May 8, 2005. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory, 2005.

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Lingner, Joachim, Dorothy Shippen, and Virginia A. Zakian. Abstracts of papers presented at the 2009 meeting on telomeres & telomerase: April 28 - May 2, 2009. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory, 2009.

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Lundblad, Victoria. Abstracts of papers presented at the 2003 meeting on telomeres & telomerase, April 30-May 4, 2003. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory, 2003.

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Mehdipour, Parvin, ed. Telomere Territory and Cancer. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-4632-9.

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Leonardo, Mancini, ed. Telomeres: Function, shortening, and lengthening. Hauppauge, NY: Nova Science Publishers, 2009.

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W, Greider Carol, and Cold Spring Harbor Laboratory, eds. Abstracts of papers presented at the 2001 meeting on telomeres & telomerase, March 28-April 1, 2001. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory, 2001.

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Dominguez, Nicolás E., and Sofia M. Pereyra. Telomeres: Biological functions, sequencing and aging. Hauppauge] New York: Nova Biomedical, Nova Science Publishers, Inc., 2012.

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H, Blackburn Elizabeth, and Greider Carol W, eds. Telomeres. Plainview, N.Y: Cold Spring Harbor Laboratory Press, 1995.

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Stivison, Elizabeth Anne. Interstitial Telomere Sequences Disrupt Break Induced Replication. [New York, N.Y.?]: [publisher not identified], 2019.

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Book chapters on the topic "Telomere"

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Joseph, Nithila A., Chi-Fan Chen, Jiun-Hong Chen, and Liuh-Yow Chen. "Monitoring Telomere Maintenance During Regeneration of Annelids." In Methods in Molecular Biology, 467–78. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2172-1_24.

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AbstractTelomere shortening is a hallmark of aging and eventually constrains the proliferative capacity of cells. The protocols discussed here are used for monitoring telomeres comprehensively in Aeolosoma viride, a model system for regeneration studies. We present methods for analyzing the activity of telomerase enzyme in regenerating tissue by telomeric repeat amplification protocol (TRAP) assay, for comparing telomere length between existing tissue and newly regenerated tissue by telomere restriction fragment (TRF) assay, as well as for visualizing telomeres by fluorescence in situ hybridization (FISH).
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Heller, Lois Jane, Celette Sugg Skinner, A. Janet Tomiyama, Elissa S. Epel, Peter A. Hall, Julia Allan, Lara LaCaille, et al. "Telomere and Telomerase." In Encyclopedia of Behavioral Medicine, 1959–60. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_68.

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Tomiyama, A. Janet, and Elissa S. Epel. "Telomere and Telomerase." In Encyclopedia of Behavioral Medicine, 2227–28. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39903-0_68.

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Tahara, Hidetoshi. "Telomere G-Overhang Length Measurement Method 2: G-Tail Telomere HPA." In Telomeres and Telomerase, 55–61. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-092-8_6.

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Tahara, Hidetoshi. "Telomere G-Overhang Length Measurement Method 2: G-Tail Telomere HPA." In Telomeres and Telomerase, 63–69. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6892-3_6.

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Libertini, Giacinto. "Telomere-Subtelomere-Telomerase System." In Encyclopedia of Gerontology and Population Aging, 1–11. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-69892-2_59-1.

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Libertini, Giacinto. "Telomere-Subtelomere-Telomerase System." In Encyclopedia of Gerontology and Population Aging, 4982–92. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-22009-9_59.

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Multani, Asha S., and Sandy Chang. "Cytogenetic Analysis of Telomere Dysfunction." In Telomeres and Telomerase, 139–43. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-092-8_13.

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Rai, Rekha, and Sandy Chang. "Probing the Telomere Damage Response." In Telomeres and Telomerase, 145–50. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-092-8_14.

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Rai, Rekha, Asha S. Multani, and Sandy Chang. "Cytogenetic Analysis of Telomere Dysfunction." In Telomeres and Telomerase, 127–31. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6892-3_12.

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Conference papers on the topic "Telomere"

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Sannikova, A. V., M. R. Sharipova, E. V. Shakirov, and L. R. Valeeva. "THE ROLE OF TRFL PROTEINS IN THE REGULATION OF TELOMERE LENGTH MARCHANTIA POLYMORPHA." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-368.

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Telomeres are nucleoprotein structures, involved in protection of the physical ends of eukaryotic chromosomes. A decisive role in maintaining telomere stability is played by specific proteins telomere complex are TRF proteins. Here, we have shown the intraspecific variability of telomere length and the involvement of TRFL protein in telolere length maintanance in a liverwort M. polymorpha as a new model plant for telomere biology studies.
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Soboleva, O. A., A. V. Torgunakova, and V. I. Minina. "TELOMERE LENGTH IN PATIENTS WITH LUNG CANCER." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-373.

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An analysis was made of the relative length of telomeres and rs2736100 polymorphic variants of the TERT gene in 123 patients diagnosed with lung cancer and 120 healthy individuals. The telomeres of cancer patients turned out to be statistically significantly longer (p<0,001) compared to healthy ones. Depending on the carriage of various variants of the TERT genotypes, there were no significant differences in telomere length in both groups.
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Liu, T., Y. Choi, M. Selman, and SH Phan. "Telomerase and Telomere Length in IPF." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2700.

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Sampl, Sandra, Doris Mejri, Christian Stern, Hui Wang, and Klaus Holzmann. "Abstract 2743: Telomere transcripts improve synthetic inhibitors of telomerase." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2743.

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Singh, Mandal K., Yehuda Tzfati, Lara J. Chensny, Panayiotis V. Benos, and Naftali Kaminski. "Regulation Telomerase and Telomere Length In IPF By MicroRNAs." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2297.

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Reddy, R., J. Lee, and B. Driscoll. "Telomerase and Telomere Length Modulate Pulmonary Response to Oxidative Stress." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4182.

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Fan, Y. L., C. Zheng, N. Wu, Y. Li, X. Huang, and Q. Ye. "Telomerase Gene Variants and Telomere Shortening in Patients with Pneumoconiosis." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7140.

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Han, S., and N. S. Chandel. "Negligible Telomere-Independent Effect of Telomerase on Alveolar Epithelial Cells." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2117.

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Yıldırım, Halime, Birsen Pınar Yıldız, and Ender Mehmet Coşkunpınar. "The study of telomere associated genes and telomere measurement in Idiopathic Pulmonary Fibrosis." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.449.

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Huang, Chenhui, Xueyu Dai, and Weihang Chai. "Abstract 2039: Human Stn1 protects telomere integrity by promoting efficient lagging strand synthesis at telomeres." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2039.

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Reports on the topic "Telomere"

1

Lundblad, Victoria. Telomere Maintenance in the Absence of Telomerase. Fort Belvoir, VA: Defense Technical Information Center, April 2000. http://dx.doi.org/10.21236/ada392106.

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Fordyca, Colleen, and Jeffrey Griffith. Telomere DNA Content, Telomerase, and c-Myc Amplification in Breast Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada396805.

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Broccoli, Dominique. Telomerase Independent Telomere Maintenance in Ovarian Cancer: A Molecular Genetic Analysis. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada407268.

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Broccoli, Dominique. Telomerase Independent Telomere Maintenance in Ovarian Cancer: A Molecular Genetic Analysis. Fort Belvoir, VA: Defense Technical Information Center, July 2004. http://dx.doi.org/10.21236/ada428241.

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Cervantes, Rachel. The Role of the Telomere End Protection Complex in Telomere Main. Fort Belvoir, VA: Defense Technical Information Center, June 2003. http://dx.doi.org/10.21236/ada437895.

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Cervantes, Rachel B. The Role of the Telomere End Protection Complex in Telomere Maintenance. Fort Belvoir, VA: Defense Technical Information Center, June 2003. http://dx.doi.org/10.21236/ada417832.

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Pennock, Erin, and Vicki Lundblad. Identification of New Genes that Regulate Telomerase and Telomere Length in Budding Yeast. Fort Belvoir, VA: Defense Technical Information Center, June 2001. http://dx.doi.org/10.21236/ada395954.

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Pennock, Erin, Joel Otero, and Vicki Lundblad. Identification of New Genes that Regulate Telomerase and Telomere Length in Budding Yeast. Fort Belvoir, VA: Defense Technical Information Center, June 2002. http://dx.doi.org/10.21236/ada408093.

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Otero, Joel. Identification of New Genes that Regulate Telomerase and Telomere Length in Budding Yeast. Fort Belvoir, VA: Defense Technical Information Center, June 2003. http://dx.doi.org/10.21236/ada420543.

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Paul, Satashree. How Early Life Stress Effects Telomeres in Later Life. Spring Library, April 2021. http://dx.doi.org/10.47496/nl.blog.25.

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