Relevant bibliographies by topics / Telomeren

Contents

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

Academic literature on the topic 'Telomeren'

Author: Grafiati
Published: 4 June 2021
Last updated: 30 January 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Telomeren.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Telomeren"

1

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

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
2

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
3

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
4

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
5

Ghadaouia, Sabrina, Marc-Alexandre Olivier, Aurélie Martinez, Tibila Kientega, Jian Qin, Patrick Lambert-Lanteigne, Guillaume B. Cardin, Chantal Autexier, Nicolas Malaquin, and Francis Rodier. "Homologous recombination-mediated irreversible genome damage underlies telomere-induced senescence." Nucleic Acids Research 49, no. 20 (November 2, 2021): 11690–707. http://dx.doi.org/10.1093/nar/gkab965.

Full text
Abstract:
Abstract Loss of telomeric DNA leads to telomere uncapping, which triggers a persistent, p53-centric DNA damage response that sustains a stable senescence-associated proliferation arrest. Here, we show that in normal cells telomere uncapping triggers a focal telomeric DNA damage response accompanied by a transient cell cycle arrest. Subsequent cell division with dysfunctional telomeres resulted in sporadic telomeric sister chromatid fusions that gave rise to next-mitosis genome instability, including non-telomeric DNA lesions responsible for a stable, p53-mediated, senescence-associated proliferation arrest. Unexpectedly, the blocking of Rad51/RPA-mediated homologous recombination, but not non-homologous end joining (NHEJ), prevented senescence despite multiple dysfunctional telomeres. When cells approached natural replicative senescence, interphase senescent cells displayed genome instability, whereas near-senescent cells that underwent mitosis despite the presence of uncapped telomeres did not. This suggests that these near-senescent cells had not yet acquired irreversible telomeric fusions. We propose a new model for telomere-initiated senescence where tolerance of telomere uncapping eventually results in irreversible non-telomeric DNA lesions leading to stable senescence. Paradoxically, our work reveals that senescence-associated tumor suppression from telomere shortening requires irreversible genome instability at the single-cell level, which suggests that interventions to repair telomeres in the pre-senescent state could prevent senescence and genome instability.
APA, Harvard, Vancouver, ISO, and other styles
6

Caslini, Corrado, James A. Connelly, Amparo Serna, Dominique Broccoli, and Jay L. Hess. "MLL Associates with Telomeres and Regulates Telomeric Repeat-Containing RNA Transcription." Molecular and Cellular Biology 29, no. 16 (June 15, 2009): 4519–26. http://dx.doi.org/10.1128/mcb.00195-09.

Full text
Abstract:
ABSTRACT Mammalian telomeres consist of TTAGGG repeats organized in nucleosomes and associated with a six-protein complex known as shelterin, which preserves telomere structure and protects chromosome ends from the cellular DNA damage response. Recent studies have found that telomeres are transcribed into telomeric UUAGGG repeat-containing RNA (TERRA) starting from subtelomeric regions. TERRA binding at telomeres appears to be involved in cis-based mechanisms of telomeric chromatin organization and maintenance. A number of histone methyltransferases (HMTs) are known to influence telomeric chromatin status; however, the regulatory mechanisms of telomere transcription are poorly understood. Here, we show that the histone 3/lysine 4 (H3/K4) HMT and the transcriptional regulator MLL associate with telomeres and contribute to their H3/K4 methylation and transcription in a telomere length-dependent manner. In human diploid fibroblasts, RNA interference-mediated MLL depletion affects telomere chromatin modification and transcription and induces the telomere damage response. Telomere uncapping through either TRF2 shelterin protein knockdown or exposure to telomere G-strand DNA oligonucleotides significantly increases the transcription of TERRA, an effect mediated by the functional cooperation between MLL and the tumor suppressor p53. In total, our findings identify a previously unrecognized role of MLL in modifying telomeric chromatin and provide evidence for the functional interaction between MLL, p53, and the shelterin complex in the regulation of telomeric transcription and stability.
APA, Harvard, Vancouver, ISO, and other styles
7

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
8

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
9

Underwood, Dana H., Coleen Carroll, and Michael J. McEachern. "Genetic Dissection of the Kluyveromyces lactis Telomere and Evidence for Telomere Capping Defects in TER1 Mutants with Long Telomeres." Eukaryotic Cell 3, no. 2 (April 2004): 369–84. http://dx.doi.org/10.1128/ec.3.2.369-384.2004.

Full text
Abstract:
ABSTRACT In the yeast Kluyveromyces lactis, the telomeres are composed of perfect 25-bp repeats copied from a 30-nucleotide RNA template defined by 5-nucleotide terminal repeats. A genetic dissection of the K. lactis telomere was performed by using mutant telomerase RNA (TER1) alleles to incorporate mutated telomeric repeats. This analysis has shown that each telomeric repeat contains several functional regions, some of which may physically overlap. Mutations in the terminal repeats of the template RNA typically lead to telomere shortening, as do mutations in the right side of the Rap1p binding site. Mutations in the left half of the Rap1p binding site, however, lead to the immediate formation of long telomeres. When mutated, the region immediately 3′ of the Rap1p binding site on the TG-rich strand of the telomere leads to telomeres that are initially short but eventually undergo extreme telomere elongation. Mutations between this region and the 3′ terminal repeat cause elevated recombination despite the presence of telomeres of nearly wild-type length. Mutants with highly elongated telomeres were further characterized and exhibit signs of telomere capping defects, including elevated levels of subtelomeric recombination and the formation of extrachromosomal and single-stranded telomeric DNA. Lengthening caused by some Rap1 binding site mutations can be suppressed by high-copy-number RAP1. Mutated telomeric repeats from a delayed elongation mutant are shown to be defective at regulating telomere length in cells with wild-type telomerase, indicating that the telomeric repeats are defective at telomere length regulation.
APA, Harvard, Vancouver, ISO, and other styles
10

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Telomeren"

1

Genest, Paul-André Joseph Jean. "Analysis of the modified DNA base J and the J-binding proteins in Leishmania." Amsterdam : Amsterdam : Nederlands Kanker Instituut / Antoni Van Leeuwenhoekziekenhuis ; Universiteit van Amsterdam [Host], 2007. http://dare.uva.nl/document/47968.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Nijjar, Tarlochan Singh. "Molecular characterization of steps involved in immortal transformation of human mammary epithelial cells." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2003. http://dare.uva.nl/document/87095.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

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

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

Schulze, Franziska. "Die Telomerlänge als Prognosefaktor in MYCN nicht-amplifizierten Neuroblastomen." Doctoral thesis, Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-200943.

Full text
Abstract:
Eines der charakteristischen Merkmale des Neuroblastoms stellt seine einzigartige biologische Heterogenität dar, die eine genaue Ausage des weiteren klinischen Verlaufes stark erschwert. Bestimmte prognostisch wirksame klinische, molekularbiologische und genetische Faktoren, wie zum Beispiel Alter bei Erstdiagnose, Tumorstadium, MYCN-Amplifikation und 1p Deletion, werden seit längerem zur Risikostratifizierung genutzt. Bereits in anderen Tumorerkrankungen konnte nun der Einfluß einer Telomerlängenveränderung auf das Gesamtüberleben von Patienten nachgewiesen werden. Telomere sichern die genomische Integrität und bestimmen maßgeblich die proliferative Kapazität jeder somatischen Zelle. Aktuelle Forschungsergebnisse legen die Vermutung nahe, dass Veränderungen der Telomerlänge auch in Neuroblastomen einen prognostischen Effekt auf das Gesamtüberleben haben. In diesem Kontext untersucht die vorliegende Arbeit den Zusammenhang zwischen Telomerlänge und Gesamtüberleben in 420 MYCN nicht-amplifizierten primären Neuroblastomen mit Erstdiagnosen von 1983-2001. Hierfür wurden die relativen Telomerlängen mithilfe einer neu etablierten monochromen multiplex q-RT-PCR ermittelt. Anschließend wurden diese sowohl mit ausgesuchten klinischen Variablen (Alter bei Erstdiagnose, Tumorstadium, Primärlokalisation des Tumors, Histologie, Geschlecht und Rezidivauftreten) korreliert als auch auf ihren Einfluß auf das Gesamt- und ereignisfreie Überleben untersucht. In Korrelation mit den klinischen Parametern konnte zwischen Alter bei Erstdiagnose und Telomerlänge ein eindeutiger Zusammenhang nachgewiesen werden. Je älter die Patienten bei Erstdiagnose, desto höher war sowohl der Anteil verlängerter Telomere als auch der extremer Telomerlängenveränderungen. Neuroblastome mit verlängerten Telomeren zeigten in der gleichen Altersgruppe ein verringertes Gesamtüberleben der betroffenen Patienten verglichen mit Neuroblastomen mit verkürzten Telomeren. Somit könnte eine Telomerlängenveränderung, insbesondere verlängerte Telomere, im klinischen Alltag als Hinweis auf einen prognostisch ungünstigen Verlauf genutzt werden.
APA, Harvard, Vancouver, ISO, and other styles
5

Marzec, Paulina. "NR2C/F telomeric association drives telomere-genome rearrangements in ALT cells." Thesis, Montpellier 2, 2013. http://www.theses.fr/2013MON20179.

Full text
Abstract:
L'immortalité cellulaire est toujours accompagnée par l'activation du mécanisme de maintien des télomères. Dans la plupart des cancers humains, ce rôle est assuré par l'enzyme télomérase. Cependant, dans 15 % des tumeurs, la télomérase n'est pas activée et les télomères sont maintenus par l'allongement alternatif des télomères (ALT), voie qui implique la recombinaison des télomères. ALT est plus fréquent dans les tumeurs provenant de tissus mésenchymateux (sarcomes), representant 40-60 % des cas, que dans les tumeurs épithéliales. Comprendre le mécanisme ALT est primordial dans les thérapies anti-cancéreuses puisque certaines drogues inhibant la télomérase conduisent souvent à l'activation de l'ALT.La voie ALT est définie par de caractéristiques typiques des télomères. Dans les cellules ALT, les recombinaisons aberrantes d'ADN ne se limitent pas aux télomères puisque les génomes sont souvent fortement réarrangés. Les liens de ces caractéristiques génomiques anormales et la maintenance des télomères atypique ne sont pas connues, mais l'instabilité du génome contribue certainement à la transformation. Notre équipe a montré que les récepteurs orphelins appartenant aux familles NR2C/F ont été trouvés enrichies dans les télomères des lignées cellulaires ALT. Nous avons proposé que ces facteurs puissent être recrutés aux télomères par liaison directe à la séquence répétée GGGTCA, un site de liaison à haute affinité pour ces protéines. Mon projet vise à comprendre (i) leur mécanisme de liaison et (ii) leur rôle, dans le processus d'ALT.Dans cette étude nous montrons que dans les sarcomes primaires humains, les télomères d'ALT sont souvent liés par des récepteurs nucléaires orphelins des sous-familles NR2C/F, en particulier dans les tumeurs au stade avancé. Ceci suggère un rôle actif de ces facteurs dans la progression tumorale ALT. En utilisant la technique de ChIP-sequencing, nous avons montré que les protéines NR2C/F se lient à une répétition directe amplifiée (DR0) aux télomères, et pas de manière significative à toute autre combinaison de motif GGGTCA. Nous avons également analysé la distribution sur tout le génome de NR2C2/F2 et TRF2, une protéine de liaison des télomères, dans des cellules ALT (-) et ALT (+). Bien qu'il n'y ait que peu de sites génomiques liés par TRF2 dans les cellules ALT (-), nous avons été surpris d'identifier plusieurs centaines de régions liées par TRF2 dans les cellules ALT (+). Plus surprenant, la grande majorité de ces régions spécifiques TRF2 ALT chevauche des sites endogènes de NR2C2/F2. Étant donné que ces sites ne contiennent généralement pas les répétitions des télomères, TRF2 est probablement recruté de façon indirecte. Conformément à cette interprétation, nous montrons que les facteurs NR2C/F entrainent un rapprochement des loci et sont responsables du regroupement atypique des télomeres dans ALT. De plus, un sous-ensemble de ces régions génomiques uniques a des additions hétérogènes des séquences télomeriques ALT, suggérant un rôle dans le recrutement des télomères par des protéines NR2C/F mais aussi une fonction de ciblage de recombinaison génomique. Systématiquement, nous trouvons que ces réarrangements des télomères/génome sont situés à proximité des motifs GGGTCA endogènes. Le caryotype spectral des lignées cellulaires ATL montre que les sites télomériques interstitielles sont fréquemment localisés aux niveaux des sites de translocations/réarrangements entre deux ou plusieurs chromosomes, ce qui est également observé dans les données de ChIPseq. Ces résultats suggèrent que les réarrangements entres les télomères et le génome pourraient participer à la formation d'un caryotype complexe ce qui caractérise environ 50% des sarcomes. De plus, l'addition de sites télomériques interstitielles dans le génome est spécifique des cellules ALT et est favorisée par les dommages de l'ADN
Cellular immortality is always accompanied by the activation of telomere maintenance mechanism. In most human cancers this role is fulfilled by the telomerase enzyme. However in 15% of tumors, telomerase is not activated and telomeres are maintained by an Alternative Lengthening of Telomeres (ALT) pathway that involves telomere-telomere recombination. Interestingly ALT is more prevalent in tumors originating from mesenchymal tissues (sarcomas), where it is present in 40-60% of cases, than in epithelial tumors. Understanding ALT maintenance is critical since inhibiting telomerase in tumors leads to the activation of ALT. The ALT pathway is operationally defined by typical telomere hallmarks. In ALT cells, aberrant DNA transactions are not restricted to telomeres since genomes are often highly rearranged. Whether these abnormal genomic features are linked to atypical telomere maintenance is not known, but genome instability is certainly contributing to transformation. We have previously shown that orphan receptors of the NR2C/F families were enriched at telomeres in ALT cell lines. We proposed that these factors could be recruited to telomeres through direct binding to the GGGTCA variant repeat, a high affinity binding site for these proteins. My project is aimed at understanding (i) their mechanism of binding and (ii) their role, if any, in the ALT process.We show that in human primary sarcomas, ALT telomeres are often bound by orphan nuclear receptors of the NR2C/F subfamilies, particularly in more advanced-stage tumors. This suggests an active role for these factors in ALT tumor progression. Using ChIP-sequencing, we show that NR2C/F proteins bind to an amplified direct repeat (DR0) at telomeres, and not significantly to any other GGGTCA motif combination. We also analyzed the genome wide distribution of NR2C2/F2 and TRF2, a telomere binding protein, in ALT(-) and in ALT(+) cells. While there are only few genomic sites bound by TRF2 in ALT(-) cells, we were surprised to identify several hundred regions bound by TRF2 in ALT(+) cells. More surprisingly, the great majority of these ALT specific TRF2 regions overlap with endogenous NR2C2/F2 sites. Since these sites usually do not contain telomere repeats, TRF2 is likely indirectly recruited. Consistent with this interpretation, we show that NR2C/F factors drive locus proximity. Moreover, a subset of these unique genomic regions harbor heterogeneous ALT telomere sequence additions, not only suggesting a telomere recruitment role for NR2C/F proteins but also a recombination targeting function in the genome. Consistently, we find these telomere/genome rearrangements are located close to endogenous GGGTCA motifs. Next, we wanted to evaluate a role of these rearrangements in formation of complex karyotype which characterize approximately 50% of sarcomas. We found by spectral karyotyping that interstitial telomeric sites are frequently located at translocation/ rearrangements sites between two or more chromosomes, which we could also observe in our ChIPseq data. Furthermore, we demonstrate that addition of interstitial telomeric sites to the genome is enhanced by DNA damage and specific for ALT genome. Therefore we conclude that NR2C/F factors target telomere proximity to defined NR2C/F regions which enables telomere-genome rearrangements under DNA damage condition. This contributes not only to efficient telomere recombination, but also it drives further genomic instability at selected NR2C/F sites.We believe we identified a new mechanism of telomere dysfunction potentially driving targeted genome instability and mediated by NR2C/F proteins in ALT cells which probably underlie complexity of sarcomas genome. Understanding the ALT mechanism allows designing NR2C/F-targeted therapies in treatment of ALT tumors and therapies for patients treated with anti-telomerase drugs to prevent ALT appearance
APA, Harvard, Vancouver, ISO, and other styles
6

Henson, Jeremy D. "The role of Alternative Lengthening of Telomeres in human cancer." University of Sydney, 2006. http://hdl.handle.net/2123/1533.

Full text
Abstract:
Doctor of Philosophy
Activation of a telomere maintenance mechanism is a vital step in the development of most cancers and provides a target for the selective killing of cancer cells. Cancers can use either telomerase or Alternative Lengthening of Telomeres (ALT) to maintain their telomeres and inhibition of either telomere maintenance mechanism can cause cancer cells to undergo senescence or apoptosis. Although telomerase inhibitors are undergoing clinical trials, on commencing this study very little was known about the role of ALT in cancer, what proteins were involved in its mechanism and regulation and how it could be targeted clinically. The primary aim of this thesis was to develop an assay for ALT suitable for examining archived tumour specimens and to begin using it to examine the prevalence and clinical significance of ALT in cancer. This assay and gene expression analysis was also used to identify genes that are involved in or associated with the activation of the ALT mechanism, to contribute towards the overall goal of an ALT cancer therapy. The ALT mechanism involves recombination mediated replication and ALT cells have a marked increase in a range of recombinational events specifically at their telomeres. Presumably, as a consequence of this the telomere lengths of ALT cells are very heterogeneous and on average long. This can be detected by terminal restriction fragment (TRF) Southern analysis, which has been used previously as the definitive test for ALT activity. However, TRF analysis requires intact genomic DNA and is unsuitable for tumour specimens which are commonly archived by paraffin embedding. Another hallmark of ALT is ALT-associated PML bodies (APBs) which are the subset of PML bodies that contain telomeric DNA. Work done in this study to consolidate APBs as a hallmark of ALT, combined with published data, showed 29/31 ALT[+], 3/31 telomerase[+] and 0/10 mortal cell lines/strains are APB[+]. The three APB[+]/telomerase[+] cell lines identified here had an order of magnitude lower frequency of APB[+] nuclei than the ALT[+] cell lines. APBs may be functionally linked to the ALT mechanism and contain the recombination proteins that are thought to be involved in the ALT mechanism. This study, in collaboration with Dr W-Q Jiang, strengthened this functional link by demonstrating that loss of ALT activity (as determined by TRF analysis) coincided with the disruption of APBs. The detection of APBs was developed into a robust assay for ALT in archived tumour specimens using a technique of combined immunofluorescence and telomere fluorescence in situ hybridisation. It was demonstrated that the APB assay concurred exactly with the standard assay for ALT (TRF analysis) in 60 tumours for which TRF analysis gave unequivocal results. The APB assay may be a more appropriate technique in the case of tumour specimen heterogeneity, which may explain why the APB assay was able to give definitive results when TRF analysis was equivocal. We demonstrated that intratumoral heterogeneity for ALT does exist and this could explain why about 3% of tumours in this study were APB[+] but with more than a ten-fold reduction in the frequency of APB[+] nuclei. This study also made the novel discovery of single stranded C-rich telomeric DNA inside APBs which potentially could be used to make the APB assay more suitable for routine pathology laboratory use. The APB assay was used to show that ALT is a significant concern for oncology. ALT was utilised in approximately one quarter of glioblastoma multiforme (GBM), one third of soft tissue sarcomas (STS) including three quarters of malignant fibrous histiocytomas (MFH), half of osteosarcomas and one tenth of non-small cell lung carcinomas (NSCLC). Furthermore, the patients with these ALT[+] tumours had poor survival; median survivals were 2 years for ALT[+] GBM, 4 years for ALT[+] STS including 3.5 years for ALT[+] MFH and 5 years for ALT[+] osteosarcoma. ALT[+] STS and osteosarcomas were also just as aggressive as their ALT[-] counterparts in terms of grade and patient outcome. ALT status was not found to be associated with response to chemotherapy in osteosarcomas or survival in STS. ALT was however, less prevalent in metastatic STS. The APB assay was a prognostic indicator for GBM and was correlated with three fold increased median survival in GBM (although this survival was still poor). ALT was more common in lower grade astrocytomas (88% ALT[+]) than GBM (24% ALT[+]) and ALT[+] GBM had an identical median age at diagnosis to that reported for secondary GBM. It is discussed that these data indicate that ALT was indirectly associated with secondary GBM and is possibly an early event in its progression from lower grade astrocytoma. This is relevant because secondary GBM have distinct genetic alterations that may facilitate activation of the ALT mechanism. Putative repressors of ALT could explain why this study found that ALT varied among the different STS subtypes. ALT was common in MFH (77%), leiomyosarcoma (62%) and liposarcoma (33%) but rare in rhabdomyosarcoma (6%) and synovial sarcoma (9%). ALT was not found in colorectal carcinoma (0/31) or thyroid papillary carcinoma (0/17) which have a high prevalence of telomerase activity and a reduced need for a telomere maintenance mechanism (low cell turnover), respectively. A yeast model of ALT predicts that one of the five human RecQ helicases may be required for ALT. Using the APB assay to test for the presence of ALT in tumours from patients with known mutations in either WRN or RECQL4 it was demonstrated that neither of these RecQ helicases is essential for ALT. Although p53 and mismatch repair (MMR) proteins have been suggested to be possible repressors of ALT, there was no apparent increase in the frequency of ALT in tumours from patients with a germline mutation in p53 codon 273 or in colorectal carcinomas that had microsatellite instability and thus MMR deficiency. Also contrary to being a repressor of ALT but consistent with its ability to interact with a protein involved in the ALT mechanism, the MMR protein MLH1, was demonstrated to be present in the APBs of an ALT[+] cell line. To further test for genes that may be involved in the ALT mechanism or associated with its activation, RNA microarray was used to compare the gene expression of 12 ALT[+] with 12 matched telomerase[+] cell lines; 240 genes were identified that were significantly differentially expressed (p<0.005) between the ALT[+] and telomerase[+] cell lines. Only DRG2 and SFNX4 were significantly differentially expressed after adjusting for the estimated false positive rate. Overall, DRG2, MGMT and SATB1 were identified as most likely to be relevant to the ALT[+] tumours and Western analysis indicated that DRG2 and MGMT levels were down-regulated after activation of ALT and up-regulated after activation of telomerase, whereas SATB1 protein levels appeared to be up-regulated after immortalisation but to a higher degree with activation of ALT compared to telomerase. Since lack of MGMT is known to be a determinant of temozolomide sensitivity in GBM, the possibility that ALT and the APB assay could be used to predict temozolomide sensitivity is discussed. The microarray data was consistent with MGMT expression being suppressed by EGF (p < 0.05), indicating that caution may be needed with combining EGFR inhibitors with temozolomide in ALT cancers. One ALT[+] cell line which did not express MGMT had TTAA sequence in its telomeres. This could possibly have resulted from mutations due to lack of MGMT expression and a possible role for MGMT in the ALT mechanism is discussed. Further analysis of the microarray data identified two groups of co-regulated genes (p < 5x10-5): CEBPA, TACC2, SFXN4, HNRPK and MGMT, and SIGIRR, LEF1, NSBP1 and SATB1. Two thirds of differentially expressed genes were down-regulated in ALT. Chromosomes 10 and 15 had a bias towards genes with lower expression in ALT while chromosomes 1, 4, 14 and X had a bias towards genes with higher expression levels in ALT. This work has developed a robust assay for ALT in tumour specimens which was then used to show the significance of ALT in sarcomas, astrocytomas and NSCLC. It has also identified genes that could possibly be molecular targets for the treatment of ALT[+] cancers.
APA, Harvard, Vancouver, ISO, and other styles
7

Elchinova, Elena Georgieva. "Analysis of the levels of monocyte subsets in patients with heart failure." Doctoral thesis, Universitat Autònoma de Barcelona, 2019. http://hdl.handle.net/10803/667760.

Full text
Abstract:
La insuficiencia cardíaca es un síndrome, caracterizado por diferentes signos y síntomas clínicos debidos a una anomalía estructural o funcional del corazón. Es una de las cardiopatías más predominantes en los países desarrollados, tanto desde el punto de vista epidemiológico como de sus manifestaciones clínicas. La insuficiencia cardíaca es un problema médico creciente relacionado con una alta tasa de hospitalización e importante mortalidad y un pronóstico desfavorable con coste socioeconómico muy elevado en todo el mundo. Los monocitos son una población heterogénea de células efectoras con funciones clave en el mantenimiento y la restauración de la integridad del tejido y del sistema inmunológico. Mediante citometria de flujo se pueden separar tres subpoblaciones de monocitos humanos distintos: clásicos (CD14 ++ / CD16–), intermedios (CD14 ++ / CD16 +) y no clásicos (CD14– / CD16 +). Poco se sabe acerca de la importancia, la relación entre los niveles de los monocitos circulantes en sangre periférica y su distribución en la insuficiencia cardíaca, incluso menos se conoce si estos parámetros podrían usarse como marcadores predictores de la progresión de la enfermedad. El objetivo principal del proyecto actual fue evaluar la relación entre los niveles y la distribución de las diferentes subpoblaciones monocitarias y la longitud de sus telómeros en pacientes con insuficiencia cardíaca y los eventos adversos, comomortalidad y hospitalización por insuficiencia cardíaca. La tesis doctoral actual describe tres estudios, respectivamente de 28, 400 y 101 pacientes ambulatorios, tratados consecutivamente en una unidad multidisciplinaria de insuficiencia cardíaca desde diciembre de 2013 hasta mayo de 2015. Todos los procedimientos del estudio se realizaron de acuerdo con todos los estándares éticos y todos los participantes proporcionaron un consentimiento informado por escrito. Se extrajeron muestras de sangre periférica de todos los pacientes para su posterior análisis mediante citometría de flujo. Las muestras se incubaron directamente con anticuerpos monoclonales con fluorocromos contra antígenos de superficie específicos de monocitos, tipo CD86 (o HLA -DR), CD14 y CD 16, y en paralelo (en 101 muestras) se analizaron marcadores genéticos (telómeros) mediante un citómetro de flujo. (BD LSRFortessa) en el Departamento de Citolatría de la IGTP. Se analizó la distribución porcentual de cada subconjunto de monocitos y también se determinó cuantitativamente su recuento de células absoluto (U/mL). Durante nuestro proyecto pudimos establecer un nuevo método de análisis conjunta de subpoblaciones de monocitos y con determinación de la longitud relativa de los telómeros, que resulto rápido, preciso y mucho más barato que otros métodos utilizados previamente. En nuestro estudio, la subpoblación intermedia se asoció de forma independiente en el análisis multivariable con mortalidad por todas las causas y con la variable compuesta (mortalidad por todas las causas o ingreso por insuficiencia cardiaca). La determinación cuantitativa del recuento de células absoluto de cada subpoblación de monocitos expresado en U/mL fue superior desde el punto de vista pronóstico al porcentaje de estas subpoblaciones. Se observó una reducción de aproximadamente el 22% en la longitud de los telómeros durante un año en los monocitos de nuestros pacientes, aunque la longitud relativa y el cambio en la longitud de los telómeros no se asociaron significativamente con los resultados. Por lo tanto, no es probable que el cambio en la longitud de los telómeros sea un biomarcador útil de la progresión de la insuficiencia cardíaca. Los monocitos y las subpoblaciones de monocitos podrían usarse en el futuro no solo como un factor predictor, sino que también podrían tomarse en consideración como parte de una terapia de inmunomodulación para los pacientes con insuficiencia cardíaca.
Heart failure is a disorder characterized by different clinical signs and symptoms due to a structural or functional anomaly of the heart. It is the most predominant heart disease in developed countries, both from epidemiological point of view and clinical implications. Indeed, it is a growing medical problem related to major hospitalization needs and high mortality, with significant economic and population burden worldwide. Established prognostic factors, such as age, sex, aetiology, comorbidities, New York Heart Association functional class, left ventricle ejection fraction, and routine laboratory markers might fail to completely and individually predict disease progression and mortality. A good risk stratification strategy is crucial as risk might be refined using several biological biomarkers of different pathophysiological processes that the former mortality risk factors do not necessarily directly reflect. That is why efficient and reliable new prognostic predictor markers are of upmost importance and relevance for the future management of the disease. Monocytes are a heterogeneous population of effector cells with key roles in the maintenance and restoration of tissue integrity. Three distinct human monocyte subsets can be identified by flow cytometry: classical (CD14++/CD16–), intermediate (CD14++/CD16+) and non-classical (CD14–/CD16+). Little is known about the importance, relationship between the levels of the circulating monocytes and their distribution in heart failure, even less if these parameters could be used as a predictor markers for the progression of the disease. The main objective of the current project was to assess the relationship between the levels and distribution of the different circulating monocyte subsets and the length of its telomeres in outpatients with heart failure with adverse events, namely mortality and heart failure hospitalizations. Three cohorts of respectively 28, 400 and 101 ambulatory patients, consecutively treated at a multidisciplinary heart failure Clinic from December 2013 to May 2015 were included in the studies described in this doctoral thesis, independently of the data of their entry into the heart failure Clinic program. All study procedures were performed in accordance with all ethical standards and all participants provided written informed consent. Peripheral blood samples of all patients were extracted for subsequent analysis by flow cytometry. The samples were incubated directly by means of monoclonal antibodies with fluorocromes against monocyte specific surface antigens, type CD86 (or HLA -DR), CD14 and CD 16 and in parallel (in 100 samples) genetic markers (telomeres) were subsequently analyzed by flow cytometer (BD LSRFortessa) in the Department of Citolatry of the IGTP. The percentage distribution of each monocyte subset was analyzed and their absolute cell count (U/mL) was also determined quantitatively. We were able to establish an innovating, accurate and much less expensive method than established ones for simultaneously measuring the different monocyte subsets and the its relative telomere length. In our study, the intermediate subset was independently associated with all-cause death and the composite end-point of all-cause death or heart failure hospitalization, in multivariable analyses. The quantitative determination of the absolute cell count of each monocyte subset expressed by U/mL was superior from the prognostic point of view than the percentage of these monocyte subsets in outpatients with Heart failure. We observed about 22% reduction in telomere length over 1 year in the monocytes of our patients, being the baseline telomere length and change in telomere length not significantly associated with outcomes. Therefore, the change in telomere length is not likely to be a useful biomarker of heart failure progression. The monocytes and monocyte subsets could be used not only as a predictor factor but also might be taken into consideration as part of an immuno-modulation therapy in the future for the heart failure patients.
APA, Harvard, Vancouver, ISO, and other styles
8

Garg, Aggarwal Mansi. "Characterization of the role of SUMO in telomere length homeostasis and overhang processing at yeast telomeres." Thesis, University of Sussex, 2017. http://sro.sussex.ac.uk/id/eprint/68661/.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Nanavaty, Vishal P. "Function of Telomere Protein RAP1 and Telomeric Transcript in Antigenic Variation in Trypanosoma Brucei." Cleveland State University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=csu1485424039406009.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Wiley, Emily A. "Yeast telomere structure : genetic analysis implicating a novel terminus-specific factor in telomeric silencing /." Thesis, Connect to this title online; UW restricted, 1996. http://hdl.handle.net/1773/6359.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Telomeren"

1

The telomere. Oxford: Oxford University Press, 1995.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Greta, Blackburn, Woynarowski Dave, and Defares, J. G. (James George), 1927-, eds. Op de drempel van onsterfelijkheid: De rol van uw telomeren voor een langer, gezonder leven. Bussum]: Strengholt Uitgeverij, 2015.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Titia, De Lange, Lundblad Vicki, and Blackburn Elizabeth H, eds. Telomeres. 2nd ed. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory Press, 2006.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Foundation, Ciba, ed. Telomeres and telomerase. Chichester: John Wiley & Sons, 1997.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Double, John A., and Michael J. Thompson. Telomeres and Telomerase. New Jersey: Humana Press, 2002. http://dx.doi.org/10.1385/1592591892.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Songyang, Zhou, ed. Telomeres and Telomerase. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6892-3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Songyang, Zhou, ed. Telomeres and Telomerase. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-092-8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

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

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Hiyama, Keiko, ed. Telomeres and Telomerase in Cancer. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-879-9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Telomeres and telomerase in cancer. New York: Springer, 2009.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Telomeren"

1

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

Full text
Abstract:
AbstractTelomere shortening is a hallmark of aging and eventually constrains the proliferative capacity of cells. The protocols discussed here are used for monitoring telomeres comprehensively in Aeolosoma viride, a model system for regeneration studies. We present methods for analyzing the activity of telomerase enzyme in regenerating tissue by telomeric repeat amplification protocol (TRAP) assay, for comparing telomere length between existing tissue and newly regenerated tissue by telomere restriction fragment (TRF) assay, as well as for visualizing telomeres by fluorescence in situ hybridization (FISH).
APA, Harvard, Vancouver, ISO, and other styles
2

Shubernetskaya, Olga S., and Alexey M. Olovnikov. "Telomeres." In Encyclopedia of Gerontology and Population Aging, 1–9. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-69892-2_58-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Gooch, Jan W. "Telomeres." In Encyclopedic Dictionary of Polymers, 927. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14932.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Shubernetskaya, Olga S., and Alexey M. Olovnikov. "Telomeres." In Encyclopedia of Gerontology and Population Aging, 4975–82. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-22009-9_58.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

O’Hara, James E., Igor UsUpensky, N. J. Bostanian, John L. Capinera, Reg Chapman, Carl S. Barfield, Marilyn E. Swisher, et al. "Telomere." In Encyclopedia of Entomology, 3730. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6359-6_2379.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Lamb, Jonathan C., Eugene V. Shakirov, and Dorothy E. Shippen. "Plant Telomeres." In Plant Cytogenetics, 143–91. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-70869-0_7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Lima-de-Faria, A. "The telomere." In One Hundred Years of Chromosome Research and What Remains to be Learned, 81–84. Dordrecht: Springer Netherlands, 2003. http://dx.doi.org/10.1007/978-94-017-0167-9_18.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Rej, Peter H., and Dan T. A. Eisenberg. "Telomere Depletion." In Encyclopedia of Evolutionary Psychological Science, 1–7. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-16999-6_2360-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Mattson, Mark P., Peisu Zhang, and Aiwu Cheng. "Telomere Neurobiology." In Neural Stem Cells, 185–96. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-133-8_15.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Marti del Moral, A., and G. Zalba Goñi. "Telomere Length." In Biomarkers in Disease: Methods, Discoveries and Applications, 1–26. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-81304-8_31-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Telomeren"

1

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Cao, En-Hua, Ai Chen, Xueguang Sun, Xiaoyan Zhang, Jingfen Qin, Dage Liu, Chen Wang, and Chunli Bai. "Formation of sequence-specific telomeric DNA loops via direct effects of psoralen-photosensitization on telomeres." In Optics and Optoelectronic Inspection and Control: Techniques, Applications, and Instruments, edited by Hong Liu and Qingming Luo. SPIE, 2000. http://dx.doi.org/10.1117/12.403922.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Heaphy, Christopher M., Michael C. Haffner, and Alan K. Meeker. "Abstract A06: A novel cell line model of the alternative lengthening of telomeres (ALT) telomere maintenance mechanism." In Abstracts: AACR Special Conference on Chromatin and Epigenetics in Cancer - June 19-22, 2013; Atlanta, GA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.cec13-a06.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Sun, Bing, Ying Wang, Krishna Kota, Yaru Shi, Salaam Motlek, Kepher Makambi, Christopher A. Loffredo, et al. "Abstract C22: Telomere length variation and frequency of short telomeres in blood lymphocytes: Novel biomarkers for lung cancer risk." In Abstracts: Twelfth Annual AACR International Conference on Frontiers in Cancer Prevention Research; Oct 27-30, 2013; National Harbor, MD. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1940-6215.prev-13-c22.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Pandita, Tej K., and Raj Pandita. "Abstract 2250: Role of single strand binding protein 1 in TERT recruitment to telomeres and in maintaining telomere G-overhangs." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2250.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Graham, Mindy K., Jacqueline Brosnan-Cashman, Anthony Rizzo, Michael Haffner, Alan Meeker, and Christopher Heaphy. "Abstract 4767: Generating and characterizing novel prostate cancer cell lines that employ the alternative lengthening of telomeres (ALT) telomere maintenance mechanism." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4767.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Brosnan-Cashman, Jacqueline A., Christopher M. Heaphy, and Alan K. Meeker. "Abstract 1467: Isolation and characterization of cancer cells containing ultrabright telomere DNA foci associated with alternative lengthening of telomeres (ALT): A novel utility for combined telomere-specific FISH and flow cytometry (Flow FISH)." 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.am2018-1467.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Telomeren"

1

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

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

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

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

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

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

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

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Robert L Ullrich and Susan Bailey. The Role of Telomere Dysfunction in Driving Genomic Instability. Office of Scientific and Technical Information (OSTI), January 2008. http://dx.doi.org/10.2172/922122.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Platz, Elizabeth A. Telomere Length as a Predictor of Aggressive Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, November 2008. http://dx.doi.org/10.21236/ada516649.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Telomeren' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography