Relevant bibliographies by topics / Telomere DNA

Academic literature on the topic 'Telomere DNA'

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Published: 6 September 2023

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Journal articles on the topic "Telomere DNA"

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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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Chan, Simon R. W. L., and Elizabeth H. Blackburn. "Telomeres and telomerase." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 359, no. 1441 (January 29, 2004): 109–22. http://dx.doi.org/10.1098/rstb.2003.1370.

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Telomeres are the protective DNA–protein complexes found at the ends of eukaryotic chromosomes. Telomeric DNA consists of tandem repeats of a simple, often G–rich, sequence specified by the action of telomerase, and complete replication of telomeric DNA requires telomerase. Telomerase is a specialized cellular ribonucleoprotein reverse transcriptase. By copying a short template sequence within its intrinsic RNA moiety, telomerase synthesizes the telomeric DNA strand running 5' to 3' towards the distal end of the chromosome, thus extending it. Fusion of a telomere, either with another telomere or with a broken DNA end, generally constitutes a catastrophic event for genomic stability. Telomerase acts to prevent such fusions. The molecular consequences of telomere failure, and the molecular contributors to telomere function, with an emphasis on telomerase, are discussed here.
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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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Natarajan, Shobhana, and Michael J. McEachern. "Recombinational Telomere Elongation Promoted by DNA Circles." Molecular and Cellular Biology 22, no. 13 (July 1, 2002): 4512–21. http://dx.doi.org/10.1128/mcb.22.13.4512-4521.2002.

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ABSTRACT Yeast mutants lacking telomerase are capable of maintaining telomeres by an alternate mechanism that depends on homologous recombination. We show here, by using Kluyveromyces lactis cells containing two types of telomeric repeats, that recombinational telomere elongation generates a repeating pattern common in most or all telomeres in survivors that retain both repeat types. We propose that these patterns arise from small circles of telomeric DNA being used as templates for rolling-circle gene conversion and that the sequence from the lengthened telomere is spread to other telomeres by additional, more typical gene conversion events. Consistent with this, artificially constructed circles of DNA containing telomeric repeats form long tandem arrays at telomeres when transformed into K. lactis cells. Mixing experiments done with two species of telomeric circles indicated that all of the integrated copies of the transforming sequence arise from a single original circular molecule.
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Evans, S. K., and V. Lundblad. "Positive and negative regulation of telomerase access to the telomere." Journal of Cell Science 113, no. 19 (October 1, 2000): 3357–64. http://dx.doi.org/10.1242/jcs.113.19.3357.

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The protective caps on chromosome ends - known as telomeres - consist of DNA and associated proteins that are essential for chromosome integrity. A fundamental part of ensuring proper telomere function is maintaining adequate length of the telomeric DNA tract. Telomeric repeat sequences are synthesized by the telomerase reverse transcriptase, and, as such, telomerase is a central player in the maintenance of steady-state telomere length. Evidence from both yeast and mammals suggests that telomere-associated proteins positively or negatively control access of telomerase to the chromosome terminus. In yeast, positive regulation of telomerase access appears to be achieved through recruitment of the enzyme by the end-binding protein Cdc13p. In contrast, duplex-DNA-binding proteins assembled along the telomeric tract exert a feedback system that negatively modulates telomere length by limiting the action of telomerase. In mammalian cells, and perhaps also in yeast, binding of these proteins probably promotes a higher-order structure that renders the telomere inaccessible to the telomerase enzyme.
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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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Natarajan, Shobhana, Cindy Groff-Vindman, and Michael J. McEachern. "Factors Influencing the Recombinational Expansion and Spread of Telomeric Tandem Arrays in Kluyveromyces lactis." Eukaryotic Cell 2, no. 5 (October 2003): 1115–27. http://dx.doi.org/10.1128/ec.2.5.1115-1127.2003.

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ABSTRACT We have previously shown that DNA circles containing telomeric repeats and a marker gene can promote the recombinational elongation of telomeres in Kluyveromyces lactis by a mechanism proposed to involve rolling-circle DNA synthesis. Wild-type cells acquire a long tandem array at a single telomere, while telomerase deletion (ter1-Δ) cells, acquire an array and also spread it to multiple telomeres. In this study, we further examine the factors that affect the formation and spread of telomeric tandem arrays. We show that a telomerase+ strain with short telomeres and high levels of subtelomeric gene conversion can efficiently form and spread arrays, while a telomere fusion mutant is not efficient at either process. This indicates that an elevated level of gene conversion near telomeres is required for spreading but that growth senescence and a tendency to elongate telomeres in the absence of exogenously added circles are not. Surprisingly, telomeric repeats are frequently deleted from a transforming URA3-telomere circle at or prior to the time of array formation by a mechanism dependent upon the presence of subtelomeric DNA in the circle. We further show that in a ter1-Δ strain, long tandem arrays can arise from telomeres initially containing a single-copy insert of the URA3-telomere sequence. However, the reduced rate of array formation in such strains suggests that single-copy inserts are not typical intermediates in arrays formed from URA3-telomere circles. Using heteroduplex circles, we have demonstrated that either strand of a URA3-telomere circle can be utilized to form telomeric tandem arrays. Consistent with this, we demonstrate that 100-nucleotide single-stranded telomeric circles of either strand can promote recombinational telomere elongation.
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Ji, Hong, Christopher J. Adkins, Bethany R. Cartwright, and Katherine L. Friedman. "Yeast Est2p Affects Telomere Length by Influencing Association of Rap1p with Telomeric Chromatin." Molecular and Cellular Biology 28, no. 7 (January 22, 2008): 2380–90. http://dx.doi.org/10.1128/mcb.01648-07.

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ABSTRACT In Saccharomyces cerevisiae, the sequence-specific binding of the negative regulator Rap1p provides a mechanism to measure telomere length: as the telomere length increases, the binding of additional Rap1p inhibits telomerase activity in cis. We provide evidence that the association of Rap1p with telomeric DNA in vivo occurs in part by sequence-independent mechanisms. Specific mutations in EST2 (est2-LT) reduce the association of Rap1p with telomeric DNA in vivo. As a result, telomeres are abnormally long yet bind an amount of Rap1p equivalent to that observed at wild-type telomeres. This behavior contrasts with that of a second mutation in EST2 (est2-up34) that increases bound Rap1p as expected for a strain with long telomeres. Telomere sequences are subtly altered in est2-LT strains, but similar changes in est2-up34 telomeres suggest that sequence abnormalities are a consequence, not a cause, of overelongation. Indeed, est2-LT telomeres bind Rap1p indistinguishably from the wild type in vitro. Taken together, these results suggest that Est2p can directly or indirectly influence the binding of Rap1p to telomeric DNA, implicating telomerase in roles both upstream and downstream of Rap1p in telomere length homeostasis.
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Kelleher, Colleen, Isabel Kurth, and Joachim Lingner. "Human Protection of Telomeres 1 (POT1) Is a Negative Regulator of Telomerase Activity In Vitro." Molecular and Cellular Biology 25, no. 2 (January 15, 2005): 808–18. http://dx.doi.org/10.1128/mcb.25.2.808-818.2005.

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ABSTRACT The telomeric single-strand DNA binding protein protection of telomeres 1 (POT1) protects telomeres from rapid degradation in Schizosaccharomyces pombe and has been implicated in positive and negative telomere length regulation in humans. Human POT1 appears to interact with telomeres both through direct binding to the 3′ overhanging G-strand DNA and through interaction with the TRF1 duplex telomere DNA binding complex. The influence of POT1 on telomerase activity has not been studied at the molecular level. We show here that POT1 negatively effects telomerase activity in vitro. We find that the DNA binding activity of POT1 is required for telomerase inhibition. Furthermore, POT1 is incapable of inhibiting telomeric repeat addition to substrate primers that are defective for POT1 binding, suggesting that in vivo, POT1 likely affects substrate access to telomerase.
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Smith, Christopher D., and Elizabeth H. Blackburn. "Uncapping and Deregulation of Telomeres Lead to Detrimental Cellular Consequences in Yeast." Journal of Cell Biology 145, no. 2 (April 19, 1999): 203–14. http://dx.doi.org/10.1083/jcb.145.2.203.

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Telomeres are the protein–nucleic acid structures at the ends of eukaryote chromosomes. Tandem repeats of telomeric DNA are templated by the RNA component (TER1) of the ribonucleoprotein telomerase. These repeats are bound by telomere binding proteins, which are thought to interact with other factors to create a higher-order cap complex that stabilizes the chromosome end. In the budding yeast Kluyveromyces lactis, the incorporation of certain mutant DNA sequences into telomeres leads to uncapping of telomeres, manifested by dramatic telomere elongation and increased length heterogeneity (telomere deregulation). Here we show that telomere deregulation leads to enlarged, misshapen “monster” cells with increased DNA content and apparent defects in cell division. However, such deregulated telomeres became stabilized at their elongated lengths upon addition of only a few functionally wild-type telomeric repeats to their ends, after which the frequency of monster cells decreased to wild-type levels. These results provide evidence for the importance of the most terminal repeats at the telomere in maintaining the cap complex essential for normal telomere function. Analysis of uncapped and capped telomeres also show that it is the deregulation resulting from telomere uncapping, rather than excessive telomere length per se, that is associated with DNA aberrations and morphological defects.
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Dissertations / Theses on the topic "Telomere DNA"

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Moye, Aaron Lavel. "Understanding the relationship between telomeres, telomerase, and DNA G-quadruplexes." Thesis, The University of Sydney, 2017. http://hdl.handle.net/2123/17713.

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Cancer cells elongate their telomeres - G-rich repetitive sequences found at the end of linear chromosomes, allowing limitless replicative potential in these cells. Approximately 85% of cancers use telomerase to extend telomeres, making it an attractive potential anti-cancer target. The G-rich nature of telomeres allows the formation of DNA G-quadruplex secondary structures. Previous data had demonstrated that telomeric G-quadruplex substrates could not be extended by ciliate telomerase (Zahler et al., 1991). However, while the above observation is true for anti-parallel G-quadruplexes, parallel G-quadruplexes were shown to be substrates for ciliate telomerase (Oganesian et al., 2006). Whether human telomerase could extend parallel G-quadruplexes was unknown. In this thesis, I confirmed that human telomerase, like ciliate telomerase, can extend parallel, intermolecular G-quadruplexes in vitro. The ability of telomerase to extend G-quadruplexes is also true for parallel, intramolecular G-quadruplexes, indicating that the parallel nature of the structure allows telomerase extension. Extension of parallel G-quadruplexes using both biochemical and single-molecule FRET microscopy revealed that parallel G-quadruplexes are bound by telomerase as a distinct substrate and partially unfolded, allowing hybridisation of the RNA template. This partially unwound G-quadruplex is extended by human telomerase to the hTR template boundary, followed by translocation and complete G-quadruplex unfolding. Stabilisation of the parallel G-quadruplex using a parallel-G-quadruplex-specific ligand NMM did not inhibit telomerase activity demonstrating that chemically-stabilised parallel G-quadruplexes can be extended by human telomerase. Using a G-quadruplex specific antibody I showed that G-quadruplexes at telomeres increased after NMM treatment, indicating that parallel G-quadruplexes exist at human telomeres in vivo, and that telomeres with G-quadruplexes are a site of localisation for human telomerase. A potential protective effect of Gquadruplexes at uncapped telomeres was also investigated. In Saccharomyces cerevisiae lacking cdc13, equivalent in function to mammalian POT1, the DNA damage response could be suppressed by stabilising Gquadruplexes, showing that G-quadruplexes can have a protective effect at uncapped telomeres, but whether this is true at mammalian telomeres was unknown. In chapter 3 of this thesis I demonstrated that the DNA damage response at uncapped telomeres was suppressed by G-quadruplex stabilising ligands in G1 cells. I showed that G-quadruplex-telomere colocalisation increase in the absence of POT1, consistent with in vitro FRET experiments (Hwang et al., 2012). Treatment of POT1-deficient telomeres in G1 with G-quadruplex stabilising ligands reduced G-quadruplex-telomeres colocalisation. I provide preliminary data indicating that the nucleotide excision repair pathway is responsible for this phenotype, and that loss of stabilised telomeric G-quadruplexes is linked to the DNA damage response suppression phenotype. This thesis provides a body of work that improves our understanding of the role of G-quadruplexes at telomeres.
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Kamnert, Iréne. "Classes of DNA associated with telomeres in the chironomids C. pallidivittatus and C. tentans." Lund : Dept. of Genetics, Lund University, 1997. http://catalog.hathitrust.org/api/volumes/oclc/39009480.html.

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Xing, Xuekun. "DNA replication and telomere resolution in vaccinia virus." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq23557.pdf.

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Ojani, Maryam. "Relationship between DNA damage response and telomere maintenance." Thesis, Brunel University, 2012. http://bura.brunel.ac.uk/handle/2438/7441.

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Telomeres are regions of repetitive DNA bound with a set of specialized proteins required to protect chromosomes from fusing with each other and from eliciting DNA damage response. Dysfunctional telomere maintenance can lead to premature cellular senescence, premature organismal aging and cancer predisposition. In the last few years the evidence has emerged indicating a link between dysfunctional maintenance of telomeres and defective DNA damage response. The objective of this project was to explore further this link by examining effects of some DNA damage response proteins on telomeres that have not been examined before and examining DNA damage response in cells in which telomeres are dysfunctional as a result of alterations in genes not directly involved in DNA damage response. We have developed a method, termed IQ-FISH, for accurate identification of average telomere length in interphase cells from individuals with defective DNA damage response. By applying IQ-FISH we could successfully measure telomere lengths in cell lines from patients that are heterozygous (+/-) and cell lines from patients or animals that are homozygous (-/-) with respect to mutations in these genes. We then analysed telomere length and function, as well as DNA damage response, in lymphoblastoid cell lines originating from BRCA1 and BRCA2 carriers (+/-) and also a single fibroblast cell line from a patient with bi-allelic mutations in BRCA2 (-/-). In addition we have analysed a mouse embryonic stem cell line in which Brca1 was deleted (Brca1-/-) by gene targeting. Our results show lack of correlation between DNA damage response and telomere maintenance in heterozygous cell lines (with the exception of one BRCA1+/- cell line) but a clear positive correlation in the case of cell lines with homozygous mutations. Finally, as a model for telomere dysfunction we have chosen cell lines from Dyskeratosis Congenita (DC) patients. DC is a rare progressive congenital disorder which results in premature aging. DC is primarily a disorder of dysfunctional telomere maintenance and we used cell lines from patients with mutations in DKC1, a gene encoding a protein termed Dyskerin which forms a part of the telomerase enzyme complex. Our results indicate that DC cells with dysfunctional DKC1 may have a dysfunctional DNA damage response.
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Carlos, A. R. "DNA damage responses to loss of telomere integrity." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:27bcf3b6-edb9-47e2-af7c-c7ba9b431572.

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Linear genomes end in characteristic structures consisting of repetitive DNA and proteins: the telomeres. These play two critical roles: on one hand they avoid the of loss of genetic information due to the incomplete replication of the chromosome ends and on the other, they provide capping structures for chromosome termini, differentiating them from double strand breaks. Telomeres contain specialized proteins (the shelterin complex), as well as proteins present elsewhere on the chromosomes (chromatin remodelling, DNA damage repair and response factors). Interestingly, several DNA damage factors are required for proper telomere maintenance, drawing a thin line between telomere protection and their recognition as broken DNA ends. Loss of telomere integrity has severe consequences for the cell, namely it can induce replicative senescence and cellular aging, or it can contribute to tumorigenesis. How telomeres are capped and how they are perceived by the cell when they become dysfunctional is essential for our understanding of the contribution of loss of telomere integrity to aging and disease. In order to unravel new factors involved in telomere maintenance, siRNA screens were performed. The optimization process has confirmed both telomeric foci and telomere dysfunction-induced foci (TIFs) as suitable readouts and the screens performed generated a list of potential candidate genes involved in telomere biology. Although some of the candidate genes tested in this work failed the validation process, other genes deserve further analysis. In addition this work also studied the role of several DNA damage factors at uncapped telomeres. Furthermore, BRCA1, CtIP and EXO1 were found to be critical for the formation of end-to-end fusions generated after TRF2 inactivation. The requirement of this proteins in this process, suggests that not only that not only the classical non-homologous end joining (C-NHEJ) pathway is active at TRF2-depelted telomeres, but emphasises the multiplicity of mechanisms that act to repair dysfunctional telomeres.
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Cabuy, Erik. "Investigations of telomere maintenance in DNA damage response defective cells and telomerase in brain tumours." Thesis, Brunel University, 2005. http://bura.brunel.ac.uk/handle/2438/5157.

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Telomeres are nucleoprotein complexes located at the end of chromosomes. They have an essential role in protecting chromosome ends. Telomerase or ALT (alternative lengthening of telomeres) mechanisms maintain telomeres by compensating natural telomeric loss. We have set up a flow-FISH method and using mouse lymphoma cell lines we identified unexpectedly the presence of subpopulations of cells with different telomere lengths. Subpopulations of cells with different telomere lengths were also observed in a human ALT and non-ALT cell line. Differences in telomere length between subpopulations of cells were significant and we term this phenomenon TELEFLUCS (TElomere LEngth FLUctuations in Cell Subpopulations). By applying flow-FISH we could successfully measure telomere lengths during replicative senescence in human primary fibroblasts with different genetic defects that confer sensitivity to ionising radiation (IR). The results from this study, based on flow-FISH and Southern hybridisation measurements, revealed an accelerated rate of telomere shortening in radiosensitive fibroblasts. We also observed accelerated telomere shortening in murine BRCA1 deficient cells, another defect conferring radiosensitivity, in comparison with a BRCA1 proficient cell line. We transiently depleted BRCA1 by siRNAs in two human mammary epithelial cell lines but could not find changes in telomere length in comparison with control cells. Cytological evidence of telomere dysfunction was observed in all radiosensitive cell lines. These results suggest that mechanisms that confer sensitivity to IR may be linked with mechanisms that cause telomere dysfunction. Furthermore, we have been able to show that human ALT positive cell lines show dysfunctional telomeres as detected by either the presence of DSBs at their telomeres or cytogenetic analysis and usually cells with dysfunctional telomeres are sensitive to IR. Finally, we assessed hTERT mRNA splicing variants and telomerase activity in brain tumours, which exhibit considerable chromosome instability suggesting that DNA repair mechanisms may be impaired. We demonstrated that high levels of hTERT mRNAs and telomerase activity correlate with proliferation rate. The presence of hTERT splice variants did not strictly correlate with absence of telomerase activity but hTERT spliced transcripts were observed in some telomerase negative brain tumours suggesting that hTERT splicing may contribute to activation of ALT mechanisms.
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Xu, Mengyuan. "The Role of Shelterin Proteins in Telomere DNA Protection and Regulation." Case Western Reserve University School of Graduate Studies / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=case1585760345643995.

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Brown, Karen E. "Telomere-directed breakage of the human Y chromosome." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260731.

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Denham, Elizabeth. "The Effects of Relocating the Ku-binding Stem-loop of Telomerase RNA on Telomere Healing Events." Thesis, Boston College, 2008. http://hdl.handle.net/2345/528.

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Thesis advisor: Anne E. Stellwagen
Thesis advisor: Clare O'Connor
In most eukaryotes, the enzyme telomerase adds telomeric DNA repeats to the 3' ends of chromosomes in order to stabilize them and protect them from degradation. In the budding yeast Saccharomyces cerevisiae, telomerase is a ribonucleoprotein complex consisting of multiple protein subunits and an approximately 1.3 kb RNA component termed TLC1. Among the various proteins involved in telomerase, Ku is a heterodimer that binds both to double-stranded DNA and to a 48 nucleotide stem loop on the TLC1 RNA. Beyond its function of extending telomeres at the ends of chromosomes, telomerase can also be instrumental in repairing double-stranded DNA breaks (DSBs) by adding telomeric repeats at the site of the break. This stabilizes the damaged chromosome, but also silences genes proximal to the break. Ku is an important factor in the recruitment of telomerase to these double stranded breaks, so this investigation explored whether TLC1 structural variants with relocated Ku-binding sites are still capable of healing chromosomes via the addition of telomeres. It was determined that the TLC1 RNA is flexible and can retain its function with relocated and additional Ku-binding stem loops
Thesis (BS) — Boston College, 2008
Submitted to: Boston College. College of Arts and Sciences
Discipline: Biology
Discipline: College Honors Program
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Tuntiwechapikul, Wirote. "Studies of a G-quadruplex-specific cleaving reagent, expansion of long repetitive DNA sequences, and a cytosine-specific alkylating aza-enediyne /." Full text (PDF) from UMI/Dissertation Abstracts International, 2001. http://wwwlib.umi.com/cr/utexas/fullcit?p3055255.

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Books on the topic "Telomere DNA"

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Brady, Catherine. Elizabeth Blackburn and the story of telomeres: Deciphering the ends of DNA. Cambridge, MA: Massachusetts Institute of Technology, 2007.

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Else, Kröner-Fresenius Symposium on Adult Stem Cells in Aging Diseases and Cancer (2013 Eisenach Germany). Adult stem cells in aging, diseases, and cancer. Basel: Karger, 2015.

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Advances in stem cell aging. Basel: Karger, 2012.

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Else Kröner-Fresenius Symposium on the Molecular Mechanisms of Adult Stem Cell Aging (1st 2009 Günzburg, Germany). Molecular mechanisms of adult stem cell aging. Edited by Rudolph K. Lenhard. Basel: Karger, 2010.

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O, Tollefsbol Trygve, ed. Epigenetics protocols. Totowa, N.J: Humana Press, 2004.

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Vaziri, Homayoun. Telomeres, DNA damage signaling molecules and cellular aging. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1998.

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G-quadruplex DNA: Methods and protocols. New York: Humana Press, 2010.

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Cano, Maria Isabel Nogueira, Richard McCulloch, and Marcelo Santos Da Silva, eds. Nuclear Genome Stability: DNA Replication, Telomere Maintenance, and DNA Repair. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-630-9.

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Elizabeth Blackburn and the Story of Telomeres: Deciphering the Ends of DNA. The MIT Press, 2007.

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Marti, Amelia, and Guillermo Zalba. Telomeres, Diet and Human Disease: Advances and Therapeutic Opportunities. Taylor & Francis Group, 2017.

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Book chapters on the topic "Telomere DNA"

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Kobryn, Kerri, and George Chaconas. "Hairpin Telomere Resolvases." In Mobile DNA III, 273–87. Washington, DC, USA: ASM Press, 2015. http://dx.doi.org/10.1128/9781555819217.ch12.

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Diehl, Malissa C., Lynne W. Elmore, and Shawn E. Holt. "Telomere Dysfunction and the DNA Damage Response." In Telomeres and Telomerase in Cancer, 87–125. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-879-9_4.

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Zhang, Zepeng, Qian Hu, and Yong Zhao. "Analysis of Telomere-Homologous DNA with Different Conformations Using 2D Agarose Electrophoresis and In-Gel Hybridization." In Telomeres and Telomerase, 197–204. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6892-3_18.

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Ishikawa, Fuyuki. "CST Complex and Telomere Maintenance." In DNA Replication, Recombination, and Repair, 389–401. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55873-6_15.

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Zakian, V. A., S. S. Wang, and R. Wellinger. "Telomere Replication in Saccharomyces cerevisiae." In DNA Replication: The Regulatory Mechanisms, 139–50. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-76988-7_13.

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Pandita, Tej K. "Telomere Metabolism and DNA Damage Response." In The DNA Damage Response: Implications on Cancer Formation and Treatment, 133–56. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-2561-6_7.

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Richter, Torsten, and Thomas von Zglinicki. "Oxidative DNA Damage and Telomere Shortening." In Oxidative Damage to Nucleic Acids, 100–108. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-72974-9_8.

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Gali, Himabindu, Emily Mason-Osann, and Rachel Litman Flynn. "Direct Visualization of DNA Replication at Telomeres Using DNA Fiber Combing Combined with Telomere FISH." In Methods in Molecular Biology, 319–25. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9500-4_22.

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Monson, Ellen K., Vincent P. Schulz, and Virginia A. Zakian. "Telomere Length Regulation by the Pif1 DNA Helicase." In Genomic Instability and Immortality in Cancer, 97–110. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5365-6_7.

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Simon, Marie-Noelle, Alkmini Kalousi, Evi Soutoglou, Vincent Géli, and Catherine Dargemont. "Nuclear Pore Complexes in DNA Repair and Telomere Maintenance." In Nuclear Pore Complexes in Genome Organization, Function and Maintenance, 201–18. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-71614-5_9.

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Conference papers on the topic "Telomere DNA"

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Samassekou, Oumar. "Abstract 2996: DNA-damaging agents disrupt telomere structure." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2996.

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Slezko, A., P. Frank-Herrmann, J. Zimmer, T. Strowitzki, and M. Krivega. "Telomere length as a marker of DNA damage." In 64. Kongress der Deutschen Gesellschaft für Gynäkologie und Geburtshilfe e. V. Georg Thieme Verlag, 2022. http://dx.doi.org/10.1055/s-0042-1757054.

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Khan, Nabiha Haleema, Zachary Schrank, Joseph Kellen, Sanjana Singh, Chike Osude, Neelu Puri, and Gagan Chhabra. "Abstract 1469: T-oligo mediates DNA damage responses by modulating telomere associated proteins and telomerase." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1469.

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Stohr, Bradley A., Lifeng Xu, and Elizabeth H. Blackburn. "Abstract B64: Telomeric DNA sequence determines the mechanism of dysfunctional telomere fusion in human cancer cells." In Abstracts: First AACR International Conference on Frontiers in Basic Cancer Research--Oct 8–11, 2009; Boston MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.fbcr09-b64.

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Zhang, Pan, Utz Herbig, and Muriel W. Lambert. "Abstract 2121: Nonerythroid alpha spectrin prevents telomere fragility after DNA interstrand crosslink damage." 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.am2012-2121.

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Hayashi, Makoto T., and Jan Karlseder. "Abstract IA20: A telomere-dependent DNA damage checkpoint induced by prolonged mitotic arrest." In Abstracts: AACR Special Conference: Cancer Susceptibility and Cancer Susceptibility Syndromes; January 29-February 1, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.cansusc14-ia20.

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Шадрина, Мария Михайловна, Николай Михайлович Немирович-Данченко, and Марина Юрьевна Ходанович. "METHOD OF IMMUNOHISTOCHEMICAL AND FLUORESCENT HYBRIDIZATION ANALYSIS." In Высокие технологии и инновации в науке: сборник избранных статей Международной научной конференции (Санкт-Петербург, Сентябрь 2020). Crossref, 2020. http://dx.doi.org/10.37539/vt187.2020.64.12.002.

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Нами разработан протокол совмещения иммуногистохимического окрашивания маркера молодых нейронов даблкортина и флуоресцентной гибридизации in situ (FISH) теломерной ДНК на криосрезах мозга толщиной 10 нм. Показано успешное применение, приводится подробный протокол окрашивания. We have developed a technique for joint staining of brain 10 nm criosections for doublecortin immunohistochemistry and telomere DNA fluorescent in situ hybridization. The successful application of the technique is shown, a timetable procedure is developed and all the reagents necessary for its implementation are written out, as well as the necessary temperature conditions are indicated.
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Ferreira, Carlos Eduardo Gomes, Matheus Antonio Pereira Costa, Rafael Leite Carvalho, and Adriana Sarmento De Oliveira. "A BIOLOGIA DO ENVELHECIMENTO: TELÔMEROS, TELOMERASE E ATIVIDADE FÍSICA (UMA REVISÃO SISTEMÁTICA)." In I Congresso Nacional On-line de Biologia Celular e Estrutural. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/1954.

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Introdução: Ao longo dos anos, mudanças na qualidade de vida vêm impactando diretamente a expectativa de vida humana. Estudos apontam certo envelhecimento mundial. Isso indica a importância de pesquisar a relação do impacto das atividades físicas no organismo e no envelhecimento, principalmente a nível celular, como em estruturas celulares consideradas possíveis marcadores: os telômeros. Compostos por uma curta e repetitiva sequência de DNA rica em guanina (5’-TTAGGG-3’)n, têm a função de proteger a integridade do DNA e a informação genética. Contudo, os telômeros são encurtados a cada ciclo celular, logo, acredita-se que estejam ligados ao envelhecimento biológico e senescência da célula. Para contornar tal situação, algumas células possuem a telomerase, enzima capaz de sintetizar DNA telomérico através de transcriptase reversa. Objetivos: Familiarizar o leitor com a questão atual dos telômeros, fornecendo informações atualizadas e integradas sobre a sua estrutura e função e a possível relação da prática de atividades físicas com seu comprimento e o envelhecimento, além de debater possíveis mecanismos de ação. Metodologia: Revisão bibliográfica a partir dos bancos de dados PubMed, MEDLINE e LILACS, adotando os seguintes indexadores, em diferentes combinações: telomere(s), telomerase, exercise, physical activity, aging, elderly. E a partir de artigos pré-selecionados foi realizada uma lista de referências. Resultados: A maioria dos estudos alega a associação entre a atividade física e o aumento do comprimento dos telômeros em idosos. No caso de jovens não há diferença significativa. Achados revelam telômeros, em média, 200 pb mais longos em indivíduos idosos que treinavam do que os sem treinamento. Estudos sugerem que atividade física moderada apresenta um efeito protetor no comprimento dos telômeros de leucócitos. Porém, a prática de exercícios de modo intenso possui efeito contrário na proteção dos telômeros. Ou seja, atividades físicas tanto em níveis baixos quanto em altos podem ser fatores que, em longo prazo, favorecem o encurtamento dos telômeros de leucócitos. Conclusão: Alguns estudos apresentam certa limitação, pois os dados sobre atividade física foram autorrelatados, podendo ser tendenciosos. E a inconsistência entre as pesquisas pode ser atribuída às diferentes etnias das amostras, aos métodos utilizados e a outras variáveis não levadas em consideração.
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Hayashi, Makoto, Anthony Cesare, James Fitzpatrick, Eros Lazzerini Denchi, and Jan Karlseder. "Abstract SY23-02: A telomere-dependent DNA damage checkpoint induced by prolonged mitotic arrest." 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-sy23-02.

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Wu, Jianchun, and David L. Crowe. "Abstract 1464: Telomere DNA damage links benign prostatic hypertrophy, intraepithelial neoplasia, and prostate cancer." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1464.

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Reports on the topic "Telomere DNA"

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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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Fordyce, Colleen A. Prognostic Value of Telomere DNA Content in Ductal Carcinoma In Situ. Fort Belvoir, VA: Defense Technical Information Center, June 2004. http://dx.doi.org/10.21236/ada428424.

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