Relevant bibliographies by topics / Human telomeric

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Human telomeric'

Author: Grafiati
Published: 10 March 2023

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Journal articles on the topic "Human telomeric"

1

Tommerup, H., A. Dousmanis, and T. de Lange. "Unusual chromatin in human telomeres." Molecular and Cellular Biology 14, no. 9 (September 1994): 5777–85. http://dx.doi.org/10.1128/mcb.14.9.5777-5785.1994.

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We report that human telomeres have an unusual chromatin structure characterized by diffuse micrococcal nuclease patterns. The altered chromatin manifested itself only in human telomeres that are relatively short (2 to 7 kb). In contrast, human and mouse telomeres with telomeric repeat arrays of 14 to 150 kb displayed a more canonical chromatin structure with extensive arrays of tightly packed nucleosomes. All telomeric nucleosomes showed a shorter repeat size than bulk nucleosomes, and telomeric mononucleosomal particles were found to be hypersensitive to micrococcal nuclease. However, telomeric nucleosomes were similar to bulk nucleosomes in the rate at which they sedimented through sucrose gradients. We speculate that mammalian telomeres have a bipartite structure with unusual chromatin near the telomere terminus and a more canonical nucleosomal organization in the proximal part of the telomere.
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Tommerup, H., A. Dousmanis, and T. de Lange. "Unusual chromatin in human telomeres." Molecular and Cellular Biology 14, no. 9 (September 1994): 5777–85. http://dx.doi.org/10.1128/mcb.14.9.5777.

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We report that human telomeres have an unusual chromatin structure characterized by diffuse micrococcal nuclease patterns. The altered chromatin manifested itself only in human telomeres that are relatively short (2 to 7 kb). In contrast, human and mouse telomeres with telomeric repeat arrays of 14 to 150 kb displayed a more canonical chromatin structure with extensive arrays of tightly packed nucleosomes. All telomeric nucleosomes showed a shorter repeat size than bulk nucleosomes, and telomeric mononucleosomal particles were found to be hypersensitive to micrococcal nuclease. However, telomeric nucleosomes were similar to bulk nucleosomes in the rate at which they sedimented through sucrose gradients. We speculate that mammalian telomeres have a bipartite structure with unusual chromatin near the telomere terminus and a more canonical nucleosomal organization in the proximal part of the telomere.
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Cook, Brandoch D., Jasmin N. Dynek, William Chang, Grigoriy Shostak, and Susan Smith. "Role for the Related Poly(ADP-Ribose) Polymerases Tankyrase 1 and 2 at Human Telomeres." Molecular and Cellular Biology 22, no. 1 (January 1, 2002): 332–42. http://dx.doi.org/10.1128/mcb.22.1.332-342.2002.

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ABSTRACT Telomere maintenance is essential for the continuous growth of tumor cells. In most human tumors telomeres are maintained by telomerase, a specialized reverse transcriptase. Tankyrase 1, a human telomeric poly(ADP-ribose) polymerase (PARP), positively regulates telomere length through its interaction with TRF1, a telomeric DNA-binding protein. Tankyrase 1 ADP-ribosylates TRF1, inhibiting its binding to telomeric DNA. Overexpression of tankyrase 1 in the nucleus promotes telomere elongation, suggesting that tankyrase 1 regulates access of telomerase to the telomeric complex. The recent identification of a closely related homolog of tankyrase 1, tankyrase 2, opens the possibility for a second PARP at telomeres. We therefore sought to establish the role of tankyrase 1 at telomeres and to determine if tankyrase 2 might have a telomeric function. We show that endogenous tankyrase 1 is a component of the human telomeric complex. We demonstrate that telomere elongation by tankyrase 1 requires the catalytic activity of the PARP domain and does not occur in telomerase-negative primary human cells. To investigate a potential role for tankyrase 2 at telomeres, recombinant tankyrase 2 was subjected to an in vitro PARP assay. Tankyrase 2 poly(ADP-ribosyl)ated itself and TRF1. Overexpression of tankyrase 2 in the nucleus released endogenous TRF1 from telomeres. These findings establish tankyrase 2 as a bona fide PARP, with itself and TRF1 as acceptors of ADP-ribosylation, and suggest the possibility of a role for tankyrase 2 at telomeres.
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Mattern, Karin A., Susan J. J. Swiggers, Alex L. Nigg, Bob Löwenberg, Adriaan B. Houtsmuller, and J. Mark J. M. Zijlmans. "Dynamics of Protein Binding to Telomeres in Living Cells: Implications for Telomere Structure and Function." Molecular and Cellular Biology 24, no. 12 (June 15, 2004): 5587–94. http://dx.doi.org/10.1128/mcb.24.12.5587-5594.2004.

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ABSTRACT Telomeric proteins have an essential role in the regulation of the length of the telomeric DNA tract and in protection against end-to-end chromosome fusion. Telomere organization and how individual proteins are involved in different telomere functions in living cells is largely unknown. By using green fluorescent protein tagging and photobleaching, we investigated in vivo interactions of human telomeric DNA-binding proteins with telomeric DNA. Our results show that telomeric proteins interact with telomeres in a complex dynamic fashion: TRF2, which has a dual role in chromosome end protection and telomere length homeostasis, resides at telomeres in two distinct pools. One fraction (∼73%) has binding dynamics similar to TRF1 (residence time of ∼44 s). Interestingly, the other fraction of TRF2 binds with similar dynamics as the putative end-protecting factor hPOT1 (residence time of ∼11 min). Our data support a dynamic model of telomeres in which chromosome end-protection and telomere length homeostasis are governed by differential binding of telomeric proteins to telomeric DNA.
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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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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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Lin, Chih-Yi Gabriela, Anna Christina Näger, Thomas Lunardi, Aleksandra Vančevska, Gérald Lossaint, and Joachim Lingner. "The human telomeric proteome during telomere replication." Nucleic Acids Research 49, no. 21 (November 8, 2021): 12119–35. http://dx.doi.org/10.1093/nar/gkab1015.

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Abstract Telomere shortening can cause detrimental diseases and contribute to aging. It occurs due to the end replication problem in cells lacking telomerase. Furthermore, recent studies revealed that telomere shortening can be attributed to difficulties of the semi-conservative DNA replication machinery to replicate the bulk of telomeric DNA repeats. To investigate telomere replication in a comprehensive manner, we develop QTIP-iPOND - Quantitative Telomeric chromatin Isolation Protocol followed by isolation of Proteins On Nascent DNA - which enables purification of proteins that associate with telomeres specifically during replication. In addition to the core replisome, we identify a large number of proteins that specifically associate with telomere replication forks. Depletion of several of these proteins induces telomere fragility validating their importance for telomere replication. We also find that at telomere replication forks the single strand telomere binding protein POT1 is depleted, whereas histone H1 is enriched. Our work reveals the dynamic changes of the telomeric proteome during replication, providing a valuable resource of telomere replication proteins. To our knowledge, this is the first study that examines the replisome at a specific region of the genome.
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Boccardi, Virginia, Luigi Cari, Giuseppe Nocentini, Carlo Riccardi, Roberta Cecchetti, Carmelinda Ruggiero, Beatrice Arosio, Giuseppe Paolisso, Utz Herbig, and Patrizia Mecocci. "Telomeres Increasingly Develop Aberrant Structures in Aging Humans." Journals of Gerontology: Series A 75, no. 2 (November 2, 2018): 230–35. http://dx.doi.org/10.1093/gerona/gly257.

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Abstract Telomeres progressively shorten with age, and it has been proposed that critically short and dysfunctional telomeres contribute to aging and aging-associated diseases in humans. For many years it was thought that telomere erosion was strictly a consequence of the “end replication problem,” or the inability of replicative polymerases to completely duplicate linear DNA ends. It is becoming increasingly evident, however, that telomere shortening of cultured human cells is also caused because of other replication defects in telomeric repeats, those that cause fragile telomeres and other aberrant telomeric structures that can be detected on metaphase chromosomes. Whether these replication defects contribute to telomere erosion also in human tissues is currently unknown. By analyzing peripheral blood mononuclear cells from a total of 35 healthy subjects ranging in age from 23 to 101 years, we demonstrated that telomeres increasingly display aberrant structures with advancing donor age. Although the percentages of fragile telomeres increased only until adulthood, the percentages of chromosomes displaying sister telomere loss and sister telomere chromatid fusions increased consistently throughout the entire human life span. Our data, therefore, suggest that telomeric replication defects other than the end replication problem contribute to aging-associated telomere erosion in humans.
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Groff-Vindman, Cindy, Anthony J. Cesare, Shobhana Natarajan, Jack D. Griffith, and Michael J. McEachern. "Recombination at Long Mutant Telomeres Produces Tiny Single- and Double-Stranded Telomeric Circles." Molecular and Cellular Biology 25, no. 11 (June 1, 2005): 4406–12. http://dx.doi.org/10.1128/mcb.25.11.4406-4412.2005.

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ABSTRACT Recombinational telomere elongation (RTE) known as alternate lengthening of telomeres is the mechanism of telomere maintenance in up to 5 to 10% of human cancers. The telomeres of yeast mutants lacking telomerase can also be maintained by recombination. Previously, we proposed the roll-and-spread model to explain this elongation in the yeast Kluveromyces lactis. This model suggests that a very small (∼100-bp) circular molecule of telomeric DNA is copied by a rolling circle event to generate a single long telomere. The sequence of this primary elongated telomere is then spread by recombination to all remaining telomeres. Here we show by two-dimensional gel analysis and electron microscopy that small circles of single- and double-stranded telomeric DNA are commonly made by recombination in a K. lactis mutant with long telomeres. These circles were found to be especially abundant between 100 and 400 bp (or nucleotides). Interestingly, the single-stranded circles consist of only the G-rich telomeric strand sequence. To our knowledge this is the first report of single-stranded telomeric circles as a product of telomere dysfunction. We propose that the small telomeric circles form through the resolution of an intratelomeric strand invasion which resembles a t-loop. Our data reported here demonstrate that K. lactis can, in at least some circumstances, make telomeric circles of the very small sizes predicted by the roll-and-spread model. The very small circles seen here are both predicted products of telomere rapid deletion, a process observed in both human and yeast cells, and predicted templates for roll-and-spread RTE.
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Calado, Rodrigo T., Solomon A. Graf, and Neal S. Young. "Telomeric Recombination in Lymphocytes Implicates ALT, an Alternative Mechanism for Telomere Length Maintenance, in Normal Human Hematopoietic Cells." Blood 110, no. 11 (November 16, 2007): 1332. http://dx.doi.org/10.1182/blood.v110.11.1332.1332.

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Abstract Telomeres are the very ends of chromosomes and protect the genome from recombination, end-to-end-fusion, and recognition as damaged DNA. Telomeres are eroded with each cell division, eventually reaching such critically short length as to cause cell cycle arrest, apoptosis, or genomic instability. In most highly proliferative cells, including hematopoietic stem cells and T lymphocytes, telomere attrition is countered by telomere extension by telomerase reverse transcriptase complex. The majority of cancer cells also express telomerase, which maintains telomere length and allows indefinite cell proliferation. However, about 10% of tumors maintain telomere length in the absence of telomerase by mechanisms collectively termed alternative lengthening of telomeres (ALT). ALT mainly acts through asymmetrical exchange of telomeric material between chromosomes or sister chromatids, producing one daughter-cell with short telomeres and a limited life-span and its sister with long telomeres and higher proliferative capacity. To date, ALT has only been reported in cancer cells or through genetic engineering of mammalian cells. Here we investigated whether ALT mechanisms were active in hematopoietic cells using chromosome orientation fluorescent in situ hybridization (CO-FISH). In standard FISH, a telomeric probe produces fours signals per chromosome, one at each end of the two chromatids. Using CO-FISH, the newly synthesized DNA strand is fragmented by BrdU incorporation and UV light exposure and then digested by exonucleases. In CO-FISH, a telomeric probe produces two signals only, one at each end of the chromosome; in the presence of telomeric recombination, the telomeric signal is split, generating more than two signals per chromosome. Peripheral blood lymphocytes from three healthy volunteers, normal human fibroblasts, K562 cells, telomerase-positive HeLa cells (known to be negative for ALT),and telomerase-negative VA13 cells (known to be positive for ALT) were investigated for telomeric sister chromatid exchange (t-SCE); at least 20 metaphases per cell type were examined. Cultured peripheral blood lymphocytes and VA13 cells both showed increased levels of telomeric sister chromatid exchange in comparison to the other cells (P=0.0001): telomeric probe generated 2.62±0.11 telomeric signals/chromosome in lymphocytes; 2.23±0.04 in VA13 cells; 2.09±0.01 in HeLa cells; 2.02±0.01 in K562 cells; and 2.02±0.01 in human skin fibroblasts. Staining incorporated-BrdU over 24 hours and evaluation of “harlequin” chromosomes point to a similar rate of genomic sister chromatid exchange in lymphocytes, VA13 cells, and HeLa cells, suggesting that high chromatid exchange is confined to the telomeric region. A physical association between promyelocytic leukemia protein (PML) and telomeres is characteristic of some ALT-positive cells, but confocal microscopy failed to co-localize the telomeric probe and anti-PML monoclonal antibody in peripheral blood lymphocytes, suggesting that t-SCE in lymphocytes is not mediated by PML. This is the first demonstration of ALT activation in normal mammalian cells. ALT may be activated in peripheral blood lymphocytes as a complementary mechanism to maintain telomere length, and may explain the differences in age-related telomere shortening observed between lymphocytes and granulocytes.
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Dissertations / Theses on the topic "Human telomeric"

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Court, R. I. "Biochemical and structural characterisation of human telomeric complexes." Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.598073.

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In humans there are two proteins that specifically bind the duplex telomeric DNA, human TTAGGG Repeat Binding Factor 1 and 2 (hTRF1 and hTRF2). Although similar in sequence and architecture, hTRF1 and hTRF2 play different roles. hTRF1 regulates telomere length while hTRF2 acts to cap telomere ends and prevents them being recognised as DNA breaks. This work has used biochemical and structural techniques to gain insights into three telomeric complexes, hTRF2 and its cofactor hRap1 and hTRF1 and hTRF2 DNA-binding domains in complex with telomeric DNA. The first part of this thesis covers the characterisation of the interaction between hTRF2 and its partner hRap1. Minimal interaction domains of hTRF2 and hRap1 were successfully defined. Constructs were then designed for use in crystallisation trials, but as yet no crystals have been attained. The second part of this thesis involves the interactions of hTRF1 and hTRF2 with telomeric DNA. Biochemical studies were carried out with the DNA-binding domains to compare binding activity. Then, hTRF1 and hTRF2 DNA-binding domains were co-crystallised with telomeric DNA fragments and their structures determined at high resolution. The structures of the two complexes are highly similar, but there are subtle differences in the details of DNA binding. The structures show that much of the sequence specificity of hTRF1 and hTRF2 is conferred by the presence of water molecules at the protein-DNA interface and that specific sequence recognition as well as binding of duplex telomeric DNA is conserved from yeasts to mammals.
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Mashimo, Tomoko. "Folding Pathways of Human Telomeric G-quadruplex Structures." 京都大学 (Kyoto University), 2011. http://hdl.handle.net/2433/142406.

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Darmanian, Artur Pavlovich Biotechnology &amp Biomolecular Sciences Faculty of Science UNSW. "Diagnosis of human sub-telomeric chromosomal deletions by Microarray." Awarded by:University of New South Wales, 2008. http://handle.unsw.edu.au/1959.4/36668.

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ABSTRACT A major cause of genetic disease is associated with chromosomal imbalances, such as deletions (subtelomeric, terminal and interstitial), duplications, and unbalanced translocations present in a particular chromosome segment. The diagnosis of many genetic diseases remains problematic. This is due in part to difficulty in detection of DNA copy number changes, when these are either too small (for conventional cytogenetics) or too large, for standard molecular approaches. From this viewpoint, the development of new screening methods with improvement of resolution is very important. Genome-wide screening at a molecular level began to appear feasible with the completion of the human genome sequence. From this beginning, high-resolution whole-genome technologies could be envisaged, to improve the diagnostic detection rate for even the smallest of chromosomal imbalances. The technique known as ???array-based comparative genomic hybridization??? (array-CGH) does allow such a high-resolution screening, by use of reference DNA probes, printed onto arrays, thus consisting of thousands of genomic clones. In this study we extensively investigated many major aspects of array-CGH technology from preparation of microarray probes and printing microarray slides, to a development of custom protocols and custom softwares for data processing and analysis. We have trailed several array types and protocols, direct and indirect DNA labelling techniques and, as a result, we have achieved the practical application which was our target at the onset of this work. This was to use a modified array-CGH method, as a robust and economical diagnostic test in detection of deletions and duplications within the human genome. The project has been successful, in terms of one very important outcome: The laboratory in which this work was done is now the leading clinical diagnostic lab in this field, in Australia???s most populous state of New South Wales. That achievement would not have been possible without a very lengthy period of developmental work, including that which comprises much of this thesis.
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Alotibi, Raniah Saleem. "Investigating the mechanisms of telomeric mutation in human cells." Thesis, Cardiff University, 2015. http://orca.cf.ac.uk/84320/.

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Telomeres are nucleoprotein structures that contain non-coding (TTAGGG) tandem repeats and associated telomere binding proteins at the end of chromosomes. As a consequence of end-replication losses, telomeres undergo gradual erosion with ongoing cell division. It is hypothesised that in addition to the end-replication problem, mutational mechanisms may contribute to telomere erosion by generating large-scale telomeric deletion events. As short dysfunctional telomeres are capable of fusion to other chromosome ends, large-scale telomeric deletions can lead to genomic instability which in turn may drive tumour progression. The primary aim of this thesis was to investigate putative mutational mechanisms that could lead to large-scale telomeric deletion. The role of oxidative stress and it potential contribution to telomere dynamics was assessed. The induction of fragility and replication inhibition at telomeres was also examined. Furthermore, the role that G-quadruplex structure within telomere repeat sequences and the possible induction of replication fork stalling and resolution as single or double stranded breaks was also considered as a mutational mechanism that could lead to telomere deletion. High-resolution analysis of telomere dynamics using Single Telomere Length Analysis (STELA), following the induction of oxidative stress in IMR90 fibroblasts, revealed that oxidative damage does not appear to affect the rate of telomere erosion, or the frequency of large-scale telomeric deletion. The data are more consistent with the view that premature senescence does not arise as a consequence of accelerated telomere erosion, but instead more likely results from stochastic DNA damage across the rest of the genome. The analysis of telomere dynamics following the induction of chromosome fragility, showed that telomere length in Seckel cell (SCK) fibroblasts were significantly different from those of untreated cells following treatments with aphidicolin with an increase in stochastic telomeric deletion. Whilst in MRC5 fibroblasts, the induction of the telomere fragility impacted on the upper to lower allele ratio, with a loss of the longer telomere length distributions. The stabilisation of G-quadruplex structures using the G-quadruplex ligand (RHPS4), together with ATRX knockdown, showed that an absence of ATRX sensitised cells to the ligand, but that the stabilisation of G-quadruplexes, did not significantly affect the telomere dynamics as determined using STELA. Taken together, the data presented in this thesis are not consistent with a role for oxidative stress, or the formation of G-quadruplex structures, in generating large-scale telomeric deletion; however telomeric mutational events may occur following the induction of chromosome fragile sites, specifically in the context of an ATR deficiency.
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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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Liu, Jing 1963. "Molecular analysis of the telomeric half of human chromosome 2q." Thesis, McGill University, 1995. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=40179.

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The first part of my thesis dealt with the physical mapping of human chromosome 2 employing the yeast artificial chromosome (YAC) cloning system. To generate a chromosome 2 YAC sublibrary, over 1,000 interspersed repetitive sequence (IRS)-PCR probes were generated and used to screen the CEPH midi YAC library and approximately 2,000 chromosome 2-specific midi YACs were identified. These YACs were divided into 223 YAC groups, i.e., sets of unordered overlapping YACs, and using publicly available contig analysis software, a tentative order of YACs within each YAC group could be established. To order YAC groups, the chromosome 2 YAC sublibrary was screened with 87 genetically mapped microsatellites and cytogenetically mapped expressed sequence tags (ESTs), and 44 YAC groups were localized along the genetic map of chromosome 2q. In addition, 16 known genes were physically linked with microsatellites within YAC groups, thus providing integration points for genetic, cytogenetic and YAC-based physical maps of chromosome 2q. In a subsequent step of the analysis, the chromosome 2 YAC mapping data created by the Whitehead Institute (WI)/MIT Genome Center were integrated into our dataset. The integrated dataset consisted of 240 YAC groups, of which 14 large groups containing both our and WL/MIT Genome Center YAC groups were located on chromosome 2q. These 14 groups consisted of 1,195 YACs, which will form the backbone for the construction of a complete YAC contig for human chromosome 2q.
The second part of my thesis dealt with the identification of genetic markers within or in the vicinity of NRAMP1, a candidate tuberculosis susceptibility locus. The human NRAMP1 gene was mapped to chromosome 2q35 by PCR analysis in a monochromosomal hybrid panel and by YAC contig analysis. Nine sequence variants and polymorphisms were identified within the NRAMP1 gene by single strand conformation analysis (SSCA), DNA sequencing and Southern analyses. Furthermore, two highly informative microsatellites, D2S104 and D2S173 were shown to be linked to NRAMP1 within a 1.5 Mbp YAC contig. Together, these markers provide molecular tools for further genetic analysis of inherited susceptibility to tuberculosis and related diseases of the macrophage.
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Green, J. "Studying the human telomeric intramolecular quadruplex using fluorescence resonance energy transfer." Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.599658.

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The work described here involves the use of fluorescence measurements to investigate the intramolecular quadruplex formed by the human telomeric repeat. By monitoring the efficiency of energy transfer between fluorophores either side of the structure, it is possible to follow the opening of the quadruplex in real time. In many of the experiments described here this opening was induced by the addition of a strand complementary to the quadruplex-forming sequence, to form a conventional duplex structure. Initial studies focused on the rate of opening of the human telomeric intramolecular quadruplex using peptide nucleic acid (PNA), an artificial nucleic acid mimic with an unchanged back-bone. It was observed that, for micromolar PNA, the rate of opening was independent of the concentration of PNA. This is probably due to the rate of opening being limited by a rearrangement of the quadruplex-forming strand that must occur before hybridisation can take place. The activation energy of opening was obtained by repeating the opening at several temperatures. One reason for the choice of a fluorescence-based technique is the great sensitivity with which such measurements can be performed. This allows the use of much lower sample concentration than would be possible with other measurements, such as circular dichroism or UV absorbance. With the correct equipment it is possible to detect the emission from single fluorescent species. These sorts of measurements remove the averaging that occurs when measuring many molecules at the same time. The use of single molecule detection was applied to the study of the human telomeric intramolecular quadruplex, for which there are two published structures. Two species were found in solution, and molecular modelling was used to propose assignments of these to known structures for this quadruplex. Finally, the interaction between the human telomeric intramolecular quadruplex and a peptide-hemicyanine conjugate ligand was investigated. In the presence of a complementary DNA strand the quadruplex opens and forms a duplex. It was observed that in the presence of sodium ions the ligand slowed down this hybridisation in a manner that allowed the determination of the binding constant between the quadruplex and the ligand. This was repeated at several temperatures in order to obtain thermodynamic and kinetic parameters for binding and hybridisation respectively. Furthermore, in the presence of potassium the ligand was observed to have no effect on the rate of hybridisation. The results of these experiments were used to suggest a structural model for binding.
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Tkac, Jan. "Detection of telomeric DNA circles in human ALT cells using rolling circle amplification." Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/15217.

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Telomeres, the nucleoprotein structures at the ends of linear chromosomes, maintain genomic stability by protecting chromosome ends from fusion, degradation, and processing by the DNA double-strand break repair machinery. Telomere shortening, which occurs naturally in somatic cells during aging, leads to cellular senescence or apoptosis. In contrast, germline cells and cancer cells acquire unlimited replicative potential by activating a telomere lengthening mechanism, generally via reactivating the enzyme telomerase reverse transcriptase. To date, drug development targeting cellular immortalization in cancer has focused on telomerase inhibition. However, in a subset of tumours and in vitro-immortalized cell lines, telomeres are maintained by homologous recombination-mediated pathways, termed alternative lengthening of telomeres (ALT). ALT tumours are expected to be refractory to anti-telomerase therapies, so the ability to rapidly and reliably screen for ALT status in tumour-derived cells is essential for guiding therapeutic strategies that target cellular immortalization. One characteristic of ALT-mediated telomere maintenance is the presence of extrachromosomal telomeric repeat-containing DNA circles (t-circles), which provide an attractive target for detection in screening applications. Current methods oft-circle detection require considerable amounts of cells, making them unsuitable for analysis of limited clinical samples. We optimized a screen for ALT status based on a novel technique of rolling circle amplification (RCA) oft-circles from extrachromosomal DNA extracts of human ALT cells. We demonstrate that RCA requires a much lower number of cells than previously established t-circle detection methods, and screening many samples can be performed in parallel, making RCA suitable for analyzing clinical samples. T-circles were reproducibly detected in human immortalized ALT cell lines, but not in telomerase-utilizing cell lines. In addition, ectopic over-expression of telomerase in an ALT cell line does not appear to affect t-circle formation. This suggests that presence of active telomerase within a cell does not inhibit all telomeric recombination reactions. The potential for RCA as a tool to screen tumour samples for ALT activity and the link between telomerase and ALT-based telomere lengthening mechanisms are discussed.
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Koirala, Deepak P. "Mechanochemistry, Transition Dynamics and Ligand-Induced Stabilization of Human Telomeric G-Quadruplexes at Single-Molecule Level." Kent State University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=kent1397919270.

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Wallaschek, Nina [Verfasser]. "Role of the herpesvirus telomeric repeats and the protein U94 in human herpesvirus 6 integration / Nina Wallaschek." Berlin : Freie Universität Berlin, 2016. http://d-nb.info/110293318X/34.

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Books on the topic "Human telomeric"

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Stauropoulos, Dimitrios James. An analysis of the interplay between telomeric factors and DNA repair proteins, in the human ALT pathway and cellular response to genomic double strand breaks. 2005.

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Moral, Amelia Marti del, and Guillermo Zalba Goñi. Telomeres Diet and Human Disease. Taylor & Francis Group, 2021.

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

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

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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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Blackburn, Elizabeth, and Elissa Epel. Telomere Effect: A Revolutionary Approach to Living Younger, Healthier, Longer. Grand Central Publishing, 2017.

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Telomere Effect: A Revolutionary Approach to Living Younger, Healthier, Longer. Orion Publishing Group, Limited, 2018.

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Gray, Doug, Carole Proctor, and Tom Kirkwood. Biological aspects of human ageing. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0001.

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At the molecular and cellular levels human ageing is characterized by the accumulation of unrepaired random damage, and an accompanying loss of function. A major source of damage is oxidative stress caused by the generation of reactive oxygen species as a by-product of respiration. DNA and proteins are both susceptible to damage but whereas DNA damage repair systems exist, faulty proteins are generally removed by protein degradation systems. During ageing these systems become less efficient and the subsequent accumulation of damaged protein promotes protein aggregation, a process which is especially problematic in the ageing brain. Other aspects of ageing include genetic and epigenetic changes, mitochondrial dysfunction, telomere shortening, and cellular senescence, all subject to stochasticity. The complexity of the biology of ageing has led to an increase in the use of systems biology approaches whereby the use of mathematical modelling and bioinformatic tools complement the more traditional experimental approaches.
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Book chapters on the topic "Human telomeric"

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Lin, Clement, and Danzhou Yang. "Human Telomeric G-Quadruplex Structures and G-Quadruplex-Interactive Compounds." In Telomeres and Telomerase, 171–96. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6892-3_17.

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Higgs, D. R., A. O. M. Wilkie, P. Vyas, M. A. Vickers, V. J. Buckle, and P. C. Harris. "Characterization of the telomeric region of human chromosome 16p." In Chromosomes Today, 35–47. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1510-0_3.

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Xu, Jun, Zhou Songyang, Dan Liu, and Hyeung Kim. "Analysis of Average Telomere Length in Human Telomeric Protein Knockout Cells Generated by CRISPR/Cas9." In Telomeres and Telomerase, 15–28. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6892-3_2.

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Barbé-Tuana, Florencia, Lucas Kich Grun, Vinícius Pierdoná, Beatriz Cristina Dias de Oliveira, Stephany Cacete Paiva, Mark Ewusi Shiburah, Vítor Luiz da Silva, Edna Gicela Ortiz Morea, Verônica Silva Fontes, and Maria Isabel Nogueira Cano. "Human Chromosome Telomeres." In Human Genome Structure, Function and Clinical Considerations, 207–43. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-73151-9_7.

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Harley, Calvin B. "Human Ageing and Telomeres." In Novartis Foundation Symposia, 129–47. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470515433.ch9.

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Abreu, Eladio, Rebecca M. Terns, and Michael P. Terns. "Visualization of Human Telomerase Localization by Fluorescence Microscopy Techniques." In Telomeres and Telomerase, 125–37. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-092-8_12.

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Liu, Dan. "Analysis of Average Telomere Length in Cultured Human Cells." In Telomeres and Telomerase, 13–19. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-092-8_2.

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Abreu, Eladio, Rebecca M. Terns, and Michael P. Terns. "Visualization of Human Telomerase Localization by Fluorescence Microscopy Techniques." In Telomeres and Telomerase, 113–25. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6892-3_11.

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Parsa, N. "Telomerase: from Aging to Human Cancers." In Telomere Territory and Cancer, 1–28. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4632-9_1.

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Woo, Jean, Ruby Yu, and Nelson Tang. "Telomeres and Physical Activity." In Telomeres, Diet and Human Disease, 103–16. Boca Raton, FL : CRC Press, 2017. | “A science publishers book.”| Includes bibliographical references and index.: CRC Press, 2017. http://dx.doi.org/10.1201/9781315152431-7.

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Conference papers on the topic "Human telomeric"

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Lin, Clement, Guanhui Wu, Kaibo Wang, Buket Onel, Saburo Sakai, and Danzhou Yang. "Abstract 1856: Targeting human telomeres by binding of epiberberine to telomeric G-quadruplex." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1856.

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Lin, Clement, Guanhui Wu, Kaibo Wang, Buket Onel, Saburo Sakai, and Danzhou Yang. "Abstract 1856: Targeting human telomeres by binding of epiberberine to telomeric G-quadruplex." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1856.

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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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Liu, Wenting, Clement Lin, Zong-wan Mao, and Danzhou Yang. "Abstract 2752: Recognition of the hybrid-1 human telomeric G-quadruplex by a platinum(II)-based compound." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-2752.

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Liu, Wenting, Clement Lin, Zong-wan Mao, and Danzhou Yang. "Abstract 2752: Recognition of the hybrid-1 human telomeric G-quadruplex by a platinum(II)-based compound." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-2752.

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Chensheng, Ma, Chan Ruth Chau-Ting, and Kwok Wai-Ming. "Ultrafast time-resolved fluorescence study on formation and excitation dynamics of human telomeric and homo-oligomeric i-motifs at neutral pH." In Asian Spectroscopy Conference 2020. Institute of Advanced Studies, Nanyang Technological University, 2020. http://dx.doi.org/10.32655/asc_8-10_dec2020.73.

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Lin, Clement, Guanhui Wu, Yong Shao, and Danzhou Yang. "Abstract 5232: The molecular basis for specific recognition of the biologically relevant hybrid-2 type human telomeric G-quadruplex by epiberberine." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5232.

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Sánchez, J. A. Mondragón, R. Garduño Juárez, Jesús Clemente-Gallardo, Pierpaolo Bruscolini, Francisco Castejón, Pablo Echenique, and José Félix Sáenz-Lorenzo. "Study on the stability of the Quadruplex DNA Structure formed by the human telomeric repeat sequence d[AG[sub 3](TTAGGG)[sub 3]]." In LARGE SCALE SIMULATIONS OF COMPLEX SYSTEMS, CONDENSED MATTER AND FUSION PLASMA: Proceedings of the BIFI2008 International Conference: Large Scale Simulations of Complex Systems, Condensed Matter and Fusion Plasma. AIP, 2008. http://dx.doi.org/10.1063/1.3033361.

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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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Sadler, J. Evan. "THE MOLECULAR BIOLOGY OF VON WILLEBRAND FACTOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643930.

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Human von Willebrand factor (vWF) is a plasma glycoprotein that is synthesized by endothelial cells and megakaryocytes, and perhaps by syncytiotrophoblast of placenta. The biosynthesis of vWF is very complex, involving proteolytic processing, glycosyla-tion, disulfide bond formation, and sulfation. Mature vWF consists of a single subunit of ∼ 250,000 daltons that is assembled into multimer ranging from dimers to species of over 10 million daltons. vWF performs its essential hemostatic function through several binding interactions, forming a bridge between specific receptors on the platelet surface and components of damaged vascular subendothelial connective tissue. Inherited deficiency of vWF, or von Willebrand disease (vWD), is the most common genetically transmitted bleeding disorder worldwide. The last two years has been a time of very rapid progress in understanding the molecular biology of vWF. Four research groups have independently isolated and sequenced the 9 kilobase full-length vWF cDNA. The predicted protein sequence has provided a foundation for understanding the biosynthetic processing of vWF, and has clarified the relationship between vWF and a 75-100 kilodalton plasma protein of unknown function, von Willebrand antigen II (vWAgll)/ vWAgll is co-distributed with vWF in endothelial cells and platelets, and is deficient in patients with vWD. The cDNA sequence of vWF shows that vWAgll is a rather large pro-peptide for vWF, explaining the biochemical and genetic association between the two proteins. vWF has a complex evolutionary history marked by many separate gene segment duplications. The primary structure of the protein contains four distinct types of repeated domains present in two to four copies each. Repeated domains account for over 90 percent of the protein sequence. This sequence provides a framework for ordering the functional domains that have been defined by protein chemistry methods. A tryptic peptide from the amino-terminus of vWF that overlaps domain D3 binds to factor VIII and also appears to bind to heparin. Peptides that include domain A1 bind to collagens, to heparin, and to platelet glycoprotein Ib. A second collagen binding site appears to lie within domain A3. The vWF cDNA has been expressed in heterologous cells to produce small amounts of functionally and structurally normal vWF, indicating that endothelial cells are not unique in their ability to process and assemble vWF multimers. Site-directed mutagenesis has been used to show that deletion of the propeptide of vWF prevents the formation of multimers. Cloned cDNA probes have been employed to isolate vWF genomic DNA from cosmid and λ-phage libraries, and the size of the vWF gene appears to be ∼ 150 kilobases. The vWF locus has been localized to human chromosome 12p12—pter. Several intragenic RFLPs have been characterized. With them, vWF has been placed on the human genetic linkage map as the most telomeric marker currently available for the short arm of chromosome 12. A second apparently homologous locus has been identified on chromosome 22, but the relationship of this locus to the authentic vWF gene is not yet known. The mechanism of vWD has been studied by Southern blotting of genomic DNA with cDNA probes in a few patients. Three unrelated pedigrees have been shown to have total deletions of the vWF gene as the cause of severe vWD (type III). This form of gene deletion appears to predispose to the development of inhibitory alloantibodies to vWF during therapy with cryoprecipitate. During the next several years recombinant DNA methods will continue to contribute our understanding of the evolution, biosynthesis, and structure-function relationships of vWF, as well as the mechanism of additional variants of vWD at the level of gene structure.
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Reports on the topic "Human telomeric"

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Butler, Kimberly S., and Jeffrey K. Griffith. The Role of Telomeric Repeat Binding Factor 1 (TRF1) in Telomere Maintenance and as a Potential Prognostic Indicator in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2005. http://dx.doi.org/10.21236/ada435804.

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Butler, Kimberly S., and Jeffrey K. Griffith. The Role of Telomeric Repeat Binding Factor 1 (TRF1) in Telomere Maintenance and as a Potential Prognostic Indicator in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2008. http://dx.doi.org/10.21236/ada502830.

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Bulter, Kimberly S., and Jeffrey K. Griffith. The Role of Telomeric Repeat Binding Factor 1 (TRF1) in Telomere Maintenance and as a Potential Prognostic Indicator in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2006. http://dx.doi.org/10.21236/ada455877.

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Bulter, Kimberly S., and Jeffrey K. Griffith. The Role of Telomeric Repeat Binding Factor 1 (TRF1) in Telomere Maintenance and as a Potential Prognostic Indicator in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2007. http://dx.doi.org/10.21236/ada471441.

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Henegariu, O., S. Artan, J. M. Greally, X.-N. Chen, J. R. Korenberg, G. H. Vance, L. Stubbs, P. Bray-Ward, and D. C. Ward. Cryptic Translocation Identification in Human and Mouse using Several Telomeric Multiplex FISH (TM-FISH) Strategies. Office of Scientific and Technical Information (OSTI), August 2003. http://dx.doi.org/10.2172/15004910.

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Wilson, John H. The Roles of Chromosome Breaks and Telomere Dynamics in the Genome Instability Associated With Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 1999. http://dx.doi.org/10.21236/ada382943.

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