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Journal articles on the topic 'Telomerase activity and'

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Published: 2 June 2025

Last updated: 31 July 2025

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1

Criscuolo, F., S. Smith, S. Zahn, B. J. Heidinger, and M. F. Haussmann. "Experimental manipulation of telomere length: does it reveal a corner-stone role for telomerase in the natural variability of individual fitness?" Philosophical Transactions of the Royal Society B: Biological Sciences 373, no. 1741 (2018): 20160440. http://dx.doi.org/10.1098/rstb.2016.0440.

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Telomeres, the non-coding ends of linear chromosomes, are thought to be an important mechanism of individual variability in performance. Research suggests that longer telomeres are indicative of better health and increased fitness; however, many of these data are correlational and whether these effects are causal are poorly understood. Experimental tests are emerging in medical and laboratory-based studies, but these types of experiments are rare in natural populations, which precludes conclusions at an evolutionary level. At the crossroads between telomere length and fitness is telomerase, an

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2

Chen, W., S. M. Chen, Y. Yu, B. K. Xiao, Z. W. Huang, and Z. Z. Tao. "Telomerase inhibition alters telomere maintenance mechanisms in laryngeal squamous carcinoma cells." Journal of Laryngology & Otology 124, no. 7 (2010): 778–83. http://dx.doi.org/10.1017/s0022215109992854.

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AbstractBackground and purpose:Telomere length must be maintained throughout cancer cell progression and proliferation. In most tumours, telomerase activity maintains telomere length. Therefore, telomerase is a target for cancer treatments. However, some cancer cells maintain telomere length through an alternative mechanism termed ‘alternative lengthening of telomeres’. To determine how telomerase inhibition relates to the initiation of the alternative lengthening of telomeres pathway, we investigated telomerase activity and telomere maintenance in Hep-2 cells with and without reduced telomera

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3

Han, Xuesheng, Alice Hirschel, Menelaos Tsapekos, Diego Perez, and David Vollmer. "In Vitro Assessment of Gold Nanoparticles on Telomerase Activity and Telomere Length in Human Fibroblasts." International Journal of Molecular Sciences 24, no. 18 (2023): 14273. http://dx.doi.org/10.3390/ijms241814273.

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Telomerase activity coincides with lengthening of the ends of chromosomes known as telomeres. Telomere length is used as a marker for cellular aging. Telomeres shorten over time as cells divide, and certain bioactive compounds such as gold nanoparticles (AuNPs) may slow the shortening of telomeres by increasing telomerase activity. The objective of the present study is to assess the effect of AuNPs on telomerase activity and telomere length in human fibroblasts. Telomerase activity was measured using enzyme-linked immunosorbent assay (ELISA) in primary human lung fibroblasts (IMR90) and using

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4

Beery, Annaliese K., Jue Lin, Joshua S. Biddle, Darlene D. Francis, Elizabeth H. Blackburn, and Elissa S. Epel. "Chronic stress elevates telomerase activity in rats." Biology Letters 8, no. 6 (2012): 1063–66. http://dx.doi.org/10.1098/rsbl.2012.0747.

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The enzyme telomerase lengthens telomeres—protective structures containing repetitive DNA sequences at chromosome ends. Telomere shortening is associated with diseases of ageing in mammals. Chronic stress has been related to shorter immune-cell telomeres, but telomerase activity under stress may be low, permitting telomere loss, or high, partially attenuating it. We developed an experimental model to examine the impacts of extended unpredictable stress on telomerase activity in male rats. Telomerase activity was 54 per cent higher in stressed rats than in controls, and associated with stress-r

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Counter, CM, J. Gupta, CB Harley, B. Leber, and S. Bacchetti. "Telomerase activity in normal leukocytes and in hematologic malignancies." Blood 85, no. 9 (1995): 2315–20. http://dx.doi.org/10.1182/blood.v85.9.2315.bloodjournal8592315.

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Telomeres are essential for function and stability of eukaryotic chromosomes. In the absence of telomerase, the enzyme that synthesizes telomeric DNA, telomeres shorten with cell division, a process thought to contribute to cell senescence and the proliferative crisis of transformed cells. We reported telomere stabilization concomitant with detection of telomerase activity in cells immortalized in vitro and in ovarian carcinoma cells, and suggested that telomerase is essential for unlimited cell proliferation. We have now examined the temporal pattern of telomerase expression in selected hemat

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6

Wang, Fang, David H. McCulloh, Kasey Chan, et al. "The Landscape of Telomere Length and Telomerase in Human Embryos at Blastocyst Stage." Genes 14, no. 6 (2023): 1200. http://dx.doi.org/10.3390/genes14061200.

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The telomere length of human blastocysts exceeds that of oocytes and telomerase activity increases after zygotic activation, peaking at the blastocyst stage. Yet, it is unknown whether aneuploid human embryos at the blastocyst stage exhibit a different profile of telomere length, telomerase gene expression, and telomerase activity compared to euploid embryos. In present study, 154 cryopreserved human blastocysts, donated by consenting patients, were thawed and assayed for telomere length, telomerase gene expression, and telomerase activity using real-time PCR (qPCR) and immunofluorescence (IF)

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7

Zhou, Jianlong, Kyoko Hidaka, and Bruce Futcher. "The Est1 Subunit of Yeast Telomerase Binds the Tlc1 Telomerase RNA." Molecular and Cellular Biology 20, no. 6 (2000): 1947–55. http://dx.doi.org/10.1128/mcb.20.6.1947-1955.2000.

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ABSTRACT Est1 is a component of yeast telomerase, and est1mutants have senescence and telomere loss phenotypes. The exact function of Est1 is not known, and it is not homologous to components of other telomerases. We previously showed that Est1 protein coimmunoprecipitates with Tlc1 (the telomerase RNA) as well as with telomerase activity. Est1 has homology to Ebs1, an uncharacterized yeast open reading frame product, including homology to a putative RNA recognition motif (RRM) of Ebs1. Deletion of EBS1 results in short telomeres. We created point mutations in a putative RRM of Est1. One mutan

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8

Ray, Alo, and Kurt W. Runge. "The C Terminus of the Major Yeast Telomere Binding Protein Rap1p Enhances Telomere Formation." Molecular and Cellular Biology 18, no. 3 (1998): 1284–95. http://dx.doi.org/10.1128/mcb.18.3.1284.

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ABSTRACT The telomeres of most organisms consist of short repeated sequences that can be elongated by telomerase, a reverse transcriptase complex that contains its own RNA template for the synthesis of telomere repeats. In Saccharomyces cerevisiae, the RAP1gene encodes the major telomere binding protein Rap1p. Here we use a quantitative telomere formation assay to demonstrate that Rap1p C termini can enhance telomere formation more than 30-fold when they are located at internal sites. This stimulation is distinct from protection from degradation. Enhancement of formation required the gene for

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9

Perera, Omesha N., Alexander P. Sobinoff, Erdahl T. Teber, et al. "Telomerase promotes formation of a telomere protective complex in cancer cells." Science Advances 5, no. 10 (2019): eaav4409. http://dx.doi.org/10.1126/sciadv.aav4409.

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Telomerase is a ribonucleoprotein complex that catalyzes addition of telomeric DNA repeats to maintain telomeres in replicating cells. Here, we demonstrate that the telomerase protein hTERT performs an additional role at telomeres that is independent of telomerase catalytic activity yet essential for telomere integrity and cell proliferation. Short-term depletion of endogenous hTERT reduced the levels of heat shock protein 70 (Hsp70-1) and the telomere protective protein Apollo at telomeres, and induced telomere deprotection and cell cycle arrest, in the absence of telomere shortening. Short-t

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10

Yehorova, M. S., D. S. Krasnienkov, V. G. Gurianov, V. Ye Kondratiuk, and V. М. Kuharskiy. "RELATIONSHIP OF TELOMERE LENGTH, TELOMERASE ACTIVITY, AND OXIDATIVE STRESS MARKERS IN PATIENTS WITH CEREBRAL ATHEROSCLEROSIS AND TYPE 2 DIABETES." Клінічна та профілактична медицина 4, no. 9-10 (2019): 117–27. http://dx.doi.org/10.31612/2616-4868.4(10).2019.06.

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The aim of study is to determine the relationship between telomere length and telomerase activity with indicators of oxidative stress in patients with stage 1-3 cerebral atherosclerosis and type 2 diabetes. Material and methods. A total clinical and instrumental study involved 161 patients with grade 1–3 CA. Telomerase activity was determined using a tandem repeat amplification protocol with real-time detection. The relative telomere lengths were measured using real-time multiplex quantitative polymerase chain reaction. Results. A comparative analysis revealed that patients with st

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11

Liu, Pan, Yaxin Zhang, and Lina Ma. "Telomere length and associated factors in older adults with hypertension." Journal of International Medical Research 47, no. 11 (2019): 5465–74. http://dx.doi.org/10.1177/0300060519882570.

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Telomeres and telomerase play important roles in the occurrence and development of hypertension. This review was performed to clarify the factors that influence telomere length and telomerase activity in older patients and elucidate the association of these factors with hypertension. A PubMed search and critical review of studies assessing the risk factors underlying the association of hypertension with telomere length and telomerase activity was performed. Telomere length and telomerase activity were found to be associated with hypertension. The factors that influence telomere length and telo

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Winkler, Thomas, Jake E. Decker, So Gun Hong, et al. "Telomere Dynamics in Pluripotent Stem Cells Derived From Patients with Telomere Diseases." Blood 118, no. 21 (2011): 51. http://dx.doi.org/10.1182/blood.v118.21.51.51.

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Abstract Abstract 51 Telomeres are ribonucleoprotein structures located at the end of linear chromosomes that serve to maintain genomic integrity and cellular proliferative capacity. In highly proliferative cells, the enzyme complex telomerase is responsible for the maintenance and elongation of telomeres, as the process of DNA replication inherently results in loss of terminal nucleotides. Critically short telomeres and deficiency in telomerase activity are etiologic contributors in the bone marrow failure syndromes, idiopathic pulmonary fibrosis, and liver cirrhosis. Although dysfunctional t

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13

Prescott, John C., and Elizabeth H. Blackburn. "Telomerase RNA Template Mutations Reveal Sequence-Specific Requirements for the Activation and Repression of Telomerase Action at Telomeres." Molecular and Cellular Biology 20, no. 8 (2000): 2941–48. http://dx.doi.org/10.1128/mcb.20.8.2941-2948.2000.

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ABSTRACT Telomeric DNA is maintained within a length range characteristic of an organism or cell type. Significant deviations outside this range are associated with altered telomere function. The yeast telomere-binding protein Rap1p negatively regulates telomere length. Telomere elongation is responsive to both the number of Rap1p molecules bound to a telomere and the Rap1p-centered DNA-protein complex at the extreme telomeric end. Previously, we showed that a specific trinucleotide substitution in the Saccharomyces cerevisiae telomerase gene (TLC1) RNA template abolished the enzymatic activit

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14

Schrank, Zachary, Nabiha Khan, Chike Osude, et al. "Oligonucleotides Targeting Telomeres and Telomerase in Cancer." Molecules 23, no. 9 (2018): 2267. http://dx.doi.org/10.3390/molecules23092267.

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Telomeres and telomerase have become attractive targets for the development of anticancer therapeutics due to their involvement in cancer cell immortality. Currently, several therapeutics have been developed that directly target telomerase and telomeres, such as telomerase inhibitors and G-quadruplex stabilizing ligands. Telomere-specific oligonucleotides that reduce telomerase activity and disrupt telomere architecture are also in development as novel anticancer therapeutics. Specifically, GRN163L and T-oligos have demonstrated promising anticancer activity in multiple cancers types via induc

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15

Mondello, Chiara, and A. Ivana Scovassi. "Telomeres, telomerase, and apoptosis." Biochemistry and Cell Biology 82, no. 4 (2004): 498–507. http://dx.doi.org/10.1139/o04-048.

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Telomeres are specialized high-order chromatin structures that cap the ends of eukaryotic chromosomes. In vertebrates, telomeric DNA is composed of repetitions of the TTAGGG hexanucleotide, is bound to a set of specific proteins, and is elongated by the reverse transcriptase enzyme telomerase. Telomerase activity is promptly detected in cells with an indefinite replicative potential, such as cancer cells, while is almost undetectable in normal cells, which are characterized by a limited life span. Mounting evidence indicates that the maintenance of telomere integrity and telomerase protect cel

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16

Pal, Jagannath, Jason Wong, Puru Nanjappa, Saem Lee, Masood Shammas, and Nikhil C. Munshi. "Inhibition of Homologous Recombination Pathway Promotes Telomere Shortening and Cell Survival without Affecting Telomerase Activity In Myeloma." Blood 116, no. 21 (2010): 786. http://dx.doi.org/10.1182/blood.v116.21.786.786.

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Abstract Abstract 786 Recombinase (RAD51) expression and homologous recombination (HR) activity are low in normal human cells including plasma cells. It is significantly induced following exposure of normal human cells to carcinogen, and is constitutively elevated in cancer cells including multiple myeloma (MM) cells. Besides its effect on genomic stability, elevated or dysregulated HR has also been implicated in telomere maintenance in tumor and immortalized cells. These cells usually lack telomerase activity and maintain telomere length by ALT mechanism (alternate lengthening of telomeres).

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17

Kelleher, Colleen, Isabel Kurth, and Joachim Lingner. "Human Protection of Telomeres 1 (POT1) Is a Negative Regulator of Telomerase Activity In Vitro." Molecular and Cellular Biology 25, no. 2 (2005): 808–18. http://dx.doi.org/10.1128/mcb.25.2.808-818.2005.

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ABSTRACT The telomeric single-strand DNA binding protein protection of telomeres 1 (POT1) protects telomeres from rapid degradation in Schizosaccharomyces pombe and has been implicated in positive and negative telomere length regulation in humans. Human POT1 appears to interact with telomeres both through direct binding to the 3′ overhanging G-strand DNA and through interaction with the TRF1 duplex telomere DNA binding complex. The influence of POT1 on telomerase activity has not been studied at the molecular level. We show here that POT1 negatively effects telomerase activity in vitro. We fin

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18

Mason, Douglas X., Elizabeth Goneska, and Carol W. Greider. "Stem-Loop IV of Tetrahymena Telomerase RNA Stimulates Processivity in trans." Molecular and Cellular Biology 23, no. 16 (2003): 5606–13. http://dx.doi.org/10.1128/mcb.23.16.5606-5613.2003.

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ABSTRACT Telomerase is a ribonucleoprotein enzyme responsible for the addition of telomeres onto the ends of chromosomes. Short or dysfunctional telomeres can lead to cell growth arrest, apoptosis, and genomic instability. Telomerase uses its RNA subunit to copy a short template region for telomere synthesis. To probe for regions of Tetrahymena telomerase RNA essential for function, we assayed 27 circularly permuted RNA deletions for telomerase in vitro activity and binding to the telomerase reverse transcriptase catalytic protein subunit. We found that stem-loop IV is required for wild-type t

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Chiang, Y. Jeffrey, Michael T. Hemann, Karen S. Hathcock, et al. "Expression of Telomerase RNA Template, but Not Telomerase Reverse Transcriptase, Is Limiting for Telomere Length Maintenance In Vivo." Molecular and Cellular Biology 24, no. 16 (2004): 7024–31. http://dx.doi.org/10.1128/mcb.24.16.7024-7031.2004.

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ABSTRACT Telomerase consists of two essential components, the telomerase RNA template (TR) and telomerase reverse transcriptase (TERT). The haplo-insufficiency of TR was recently shown to cause one form of human dyskeratosis congenita, an inherited disease marked by abnormal telomere shortening. Consistent with this finding, we recently reported that mice heterozygous for inactivation of mouse TR exhibit a similar haplo-insufficiency and are deficient in the ability to elongate telomeres in vivo. To further assess the genetic regulation of telomerase activity, we have compared the abilities of

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Bertuch, Alison A., and Victoria Lundblad. "EXO1 Contributes to Telomere Maintenance in Both Telomerase-Proficient and Telomerase-Deficient Saccharomyces cerevisiae." Genetics 166, no. 4 (2004): 1651–59. http://dx.doi.org/10.1093/genetics/166.4.1651.

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Abstract Previous work in budding yeast has indicated that telomeres are protected, at least in part, from the action of Exo1, which degrades the C-rich strand of partially uncapped telomeres. To explore this further, we examined the consequences of Exo1-mediated activity in strains that lacked Ku, telomerase, or both. Loss of Exo1 partially rescued the telomere length defect in a yku80Δ strain, demonstrating that exonuclease action can directly contribute to telomere shortening. The rapid loss of inviability displayed by a yku80Δ est2Δ strain was also partially alleviated by an exo1Δ mutation

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Feigon, Juli. "Structural biology of telomerase mechanism and interactions at telomeres." Structural Dynamics 12, no. 2_Supplement (2025): A201. https://doi.org/10.1063/4.0000509.

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Telomerase is a unique RNA-containing reverse transcriptase that synthesizes the DNA at the 3’-ends of telomeres, the structures at the ends of linear chromosomes. It is a highly regulated determinant of tumorigenesis, cellular aging, and stem cell renewal. All telomerases contain a catalytic core comprising telomerase reverse transcriptase (TERT) and telomerase RNA (TER), along with other proteins involved in biogenesis, assembly, and activation. TER includes a template complementary to ∼1.5 telomere repeats used by TERT to repetitively synthesize the telomere repeat (dTTGGGG in Tetrahymena,

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Cong, Yu-Sheng, Woodring E. Wright, and Jerry W. Shay. "Human Telomerase and Its Regulation." Microbiology and Molecular Biology Reviews 66, no. 3 (2002): 407–25. http://dx.doi.org/10.1128/mmbr.66.3.407-425.2002.

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SUMMARY The telomere is a special functional complex at the end of linear eukaryotic chromosomes, consisting of tandem repeat DNA sequences and associated proteins. It is essential for maintaining the integrity and stability of linear eukaryotic genomes. Telomere length regulation and maintenance contribute to normal human cellular aging and human diseases. The synthesis of telomeres is mainly achieved by the cellular reverse transcriptase telomerase, an RNA-dependent DNA polymerase that adds telomeric DNA to telomeres. Expression of telomerase is usually required for cell immortalization and

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Perrem, Kilian, Lorel M. Colgin, Axel A. Neumann, Thomas R. Yeager, and Roger R. Reddel. "Coexistence of Alternative Lengthening of Telomeres and Telomerase in hTERT-Transfected GM847 Cells." Molecular and Cellular Biology 21, no. 12 (2001): 3862–75. http://dx.doi.org/10.1128/mcb.21.12.3862-3875.2001.

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ABSTRACT It has been shown previously that some immortalized human cells maintain their telomeres in the absence of significant levels of telomerase activity by a mechanism referred to as alternative lengthening of telomeres (ALT). Cells utilizing ALT have telomeres of very heterogeneous length, ranging from very short to very long. Here we report the effect of telomerase expression in the ALT cell line GM847. Expression of exogenous hTERT in GM847 (GM847/hTERT) cells resulted in lengthening of the shortest telomeres; this is the first evidence that expression of hTERT in ALT cells can induce

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Toupance, Simon, Anne-Julie Fattet, Simon N. Thornton, Athanase Benetos, Jean-Louis Guéant, and Isabelle Koscinski. "Ovarian Telomerase and Female Fertility." Biomedicines 9, no. 7 (2021): 842. http://dx.doi.org/10.3390/biomedicines9070842.

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Women’s fertility is characterized both quantitatively and qualitatively mainly by the pool of ovarian follicles. Monthly, gonadotropins cause an intense multiplication of granulosa cells surrounding the oocyte. This step of follicular development requires a high proliferation ability for these cells. Telomere length plays a crucial role in the mitotic index of human cells. Hence, disrupting telomere homeostasis could directly affect women’s fertility. Strongly expressed in ovaries, telomerase is the most effective factor to limit telomeric attrition and preserve ovarian reserve. Considering t

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Roeth, Alexander, Jan Duerig, Heike Himmelreich, et al. "T-Cells with Extremely Short Telomeres and High Telomerase Activity in T-Cell Prolymphocytic Leukemia (T-PLL): The Ideal Target for Telomerase Inhibition." Blood 108, no. 11 (2006): 497. http://dx.doi.org/10.1182/blood.v108.11.497.497.

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Abstract T-cell prolymphocytic leukemia (T-PLL) is a rare aggressive lymphoproliferative disease characterized by the expansion of a T-cell clone derived from immuno-competent post-thymic T-lymphocytes. Important mechanisms involved in expansion of human malignant cells are reactivation of telomerase, an enzyme complex, which is able to compensate the loss of telomere repeats by cell division, and maintenance or elongation of telomere length. To investigate the role of telomeres and telomerase we measured telomere length by automated multicolor flow-FISH and telomerase activity by telomeric re

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Han, Fang, Farooq Riaz, Jincheng Pu, et al. "Connecting the Dots: Telomere Shortening and Rheumatic Diseases." Biomolecules 14, no. 10 (2024): 1261. http://dx.doi.org/10.3390/biom14101261.

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Telomeres, repetitive sequences located at the extremities of chromosomes, play a pivotal role in sustaining chromosomal stability. Telomerase is a complex enzyme that can elongate telomeres by appending telomeric repeats to chromosome ends and acts as a critical factor in telomere dynamics. The gradual shortening of telomeres over time is a hallmark of cellular senescence and cellular death. Notably, telomere shortening appears to result from the complex interplay of two primary mechanisms: telomere shelterin complexes and telomerase activity. The intricate interplay of genetic, environmental

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Wells, Trystan B., Guanglei Zhang, Zenon Harley, and Homayoun Vaziri. "Genetic Hypervariability in Two Distinct Deuterostome Telomerase Reverse Transcriptase Genes and their Early Embryonic Functions." Molecular Biology of the Cell 20, no. 1 (2009): 464–80. http://dx.doi.org/10.1091/mbc.e08-07-0748.

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Functional proteins of complex eukaryotes within the same species are rather invariant. A single catalytic component of telomerase TERT is essential for an active telomerase complex that maintains telomeres. Surprisingly, we have identified two paralogous SpTERT-L and SpTERT-S genes with novel domains in Strongylocentrotus purpuratus (purple sea urchin). The SpTERT-S and SpTERT-L genes were differentially expressed throughout embryogenesis. An unusual germline nucleotide substitution and amino acid variation was evident in these TERTs. The hypervariability of SpTERT-S haplotypes among differen

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Armbruster, Blaine N., Katherine T. Etheridge, Dominique Broccoli, and Christopher M. Counter. "Putative Telomere-Recruiting Domain in the Catalytic Subunit of Human Telomerase." Molecular and Cellular Biology 23, no. 9 (2003): 3237–46. http://dx.doi.org/10.1128/mcb.23.9.3237-3246.2003.

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ABSTRACT Telomerase, the enzyme that elongates telomeres, is essential to maintain telomere length and to immortalize most cancer cells. However, little is known about the regulation of this enzyme in higher eukaryotes. We previously described a domain in the hTERT telomerase catalytic subunit that is essential for telomere elongation and cell immortalization in vivo but dispensable for catalytic activity in vitro. Here, we show that fusions of hTERT containing different mutations in this domain to the telomere binding protein hTRF2 redirected the mutated hTERT to telomeres and rescued its in

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de la Guardia, Rafael Díaz, Carolina Elosua, Purificación Catalina, et al. "Expression Profile and up-Regulation of Telomere-Associated Proteins In Multiple Myeloma." Blood 116, no. 21 (2010): 4050. http://dx.doi.org/10.1182/blood.v116.21.4050.4050.

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Abstract Abstract 4050 The role of the telomeres in the mechanisms of ageing and carcinogenesis has generated a considerable interest as a novel approach to the treatment of many cancers. Telomeres are nucleoproteins structures that protect the ends of eukaryotic chromosomes, which are particularly vulnerable due to progressive shortening in almost all dividing cells. The telomere length was observed as a critical factor in the initiation and progression of human cancers, and it is associated to chromosomal instability. Most immortal cells possess enzymatic activity of telomerase. This suggest

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Shammas, Masood A., Hemant Koley, Alexi Protopopov, et al. "Telomerase Inhibition, Telomere Shortening and Apoptotic Cell Death in Multiple Myeloma Cells Following Exposure to a Novel and Potent Telomerase Inhibitor (GRN163L), Targeting RNA component of Telomerase." Blood 104, no. 11 (2004): 638. http://dx.doi.org/10.1182/blood.v104.11.638.638.

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Abstract Telomeres, the specialized nucleoprotein structures at the ends of chromo-somes, shorten at each DNA replication, and if unopposed leads to chromosomal erosion and cell death. Telomere shortening below a critical length is prevented by telomerase. We have previously observed elevated telomerase activity and shortened telomeres in multiple myeloma (MM), making the telomere maintenance mechanism an important target for therapy. Based on success with other non-specific telomerase inhibitors, in this study, we evaluated the effects of a thio-phosphoramidate oligonucleotide specifically ta

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Rubtsova, M. P., D. P. Vasilkova, A. N. Malyavko, Yu V. Naraikina, M. I. Zvereva, and O. A. Dontsova. "Telomere Lengthening and Other Functions of Telomerase." Acta Naturae 4, no. 2 (2012): 44–61. http://dx.doi.org/10.32607/20758251-2012-4-2-44-61.

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Telomerase is an enzyme that maintains the length of the telomere. The telomere length specifies the number of divisions a cell can undergo before it finally dies (i.e. the proliferative potential of cells). For example, telomerase is activated in embryonic cell lines and the telomere length is maintained at a constant level; therefore, these cells have an unlimited fission potential. Stem cells are characterized by a lower telomerase activity, which enables only partial compensation for the shortening of telomeres. Somatic cells are usually characterized by the absence of telomerase activity.

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Rubtsova, M. P., D. P. Vasilkova, A. N. Malyavko, Yu V. Naraikina, M. I. Zvereva, and O. A. Dontsova. "Telomere Lengthening and Other Functions of Telomerase." Acta Naturae 4, no. 2 (2012): 44–61. http://dx.doi.org/10.32607/actanaturae.10630.

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Telomerase is an enzyme that maintains the length of the telomere. The telomere length specifies the number of divisions a cell can undergo before it finally dies (i.e. the proliferative potential of cells). For example, telomerase is activated in embryonic cell lines and the telomere length is maintained at a constant level; therefore, these cells have an unlimited fission potential. Stem cells are characterized by a lower telomerase activity, which enables only partial compensation for the shortening of telomeres. Somatic cells are usually characterized by the absence of telomerase activity.

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Escribano, Amparo, Sara Pastor, Ana Reula та ін. "Accelerated telomere attrition in children and teenagers with α1-antitrypsin deficiency". European Respiratory Journal 48, № 2 (2016): 350–58. http://dx.doi.org/10.1183/13993003.00176-2016.

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Numerous studies have shown that oxidative stress accelerates telomere shortening in several lung pathologies. Since oxidative stress is involved in the pathophysiology of α1-antitrypsin deficiency (AATD), we hypothesised that telomere shortening would be accelerated in AATD patients. This study aimed to assess telomere length in AATD patients and to study its association with α1-antitrypsin phenotypes.Telomere length, telomerase activity, telomerase reverse transcriptase (hTERT) expression and biomarkers of oxidative stress were measured in 62 children and teenagers (aged 2–18 years) diagnose

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Webb, Christopher J., and Virginia A. Zakian. "Telomerase RNA stem terminus element affects template boundary element function, telomere sequence, and shelterin binding." Proceedings of the National Academy of Sciences 112, no. 36 (2015): 11312–17. http://dx.doi.org/10.1073/pnas.1503157112.

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The stem terminus element (STE), which was discovered 13 y ago in human telomerase RNA, is required for telomerase activity, yet its mode of action is unknown. We report that the Schizosaccharomyces pombe telomerase RNA, TER1 (telomerase RNA 1), also contains a STE, which is essential for telomere maintenance. Cells expressing a partial loss-of-function TER1 STE allele maintained short stable telomeres by a recombination-independent mechanism. Remarkably, the mutant telomere sequence was different from that of wild-type cells. Generation of the altered sequence is explained by reverse transcri

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Drapkina, O. M., та R. N. Shepel. "THE MODERN CONCEPTION OF THE PROPER ROLE OF TELOMERЕS AND TELOMERASE IN PATHOGENESIS OF HYPERTENSION". "Arterial’naya Gipertenziya" ("Arterial Hypertension") 19, № 4 (2013): 280–98. http://dx.doi.org/10.18705/1607-419x-2013-19-4-280-298.

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In this era of high-tech medicine, scientists have the opportunity to discover previously unknown mechanisms of development throughout the course and outcome of the disease. These methods include a highly informative study of telomerase activity and telomere length measurement in hypertension. The change of the telomere length in cells relects the processes of the development and degradation of cells, as well as the stages of their life cycle. The study of genetic defects in telomeres and telomere repair mechanisms are of great practical importance for treatment approaches and making prognosis

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Bazdiara, Ioanna, Despina Pantelidou, Athanasios Anastasiadis, et al. "Dynamics of Telomere Length and Telomerase Activity in Ph1-Negative Chronic Myeloproliferative Disorders." Blood 112, no. 11 (2008): 2789. http://dx.doi.org/10.1182/blood.v112.11.2789.2789.

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Abstract Evolving data demonstrate the pathogenetic significance of chromosomal ends telomeres and telomerase activity in the molecular pathogenesis of many hematological disorders. Furthermore, the presence of eroded telomeres and enhanced telomerase activity in hematopoietic cells has been associated with poor prognosis both in myeloid and lymphoid malignancies. The aim of the present study was to evaluate telomere length and telomerase activity in patients with Ph1-negative Chronic Myeloproliferative Disorders (Ph−-CMPD) either at diagnosis or during the course of the disease and to assess

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Donate, Luis E., and Maria A. Blasco. "Telomeres in cancer and ageing." Philosophical Transactions of the Royal Society B: Biological Sciences 366, no. 1561 (2011): 76–84. http://dx.doi.org/10.1098/rstb.2010.0291.

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Telomeres protect the chromosome ends from unscheduled DNA repair and degradation. Telomeres are heterochromatic domains composed of repetitive DNA (TTAGGG repeats) bound to an array of specialized proteins. The length of telomere repeats and the integrity of telomere-binding proteins are both important for telomere protection. Furthermore, telomere length and integrity are regulated by a number of epigenetic modifications, thus pointing to higher order control of telomere function. In this regard, we have recently discovered that telomeres are transcribed generating long, non-coding RNAs, whi

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Ullah, Mujib, and Zhongjie Sun. "Klotho Deficiency Accelerates Stem Cells Aging by Impairing Telomerase Activity." Journals of Gerontology: Series A 74, no. 9 (2018): 1396–407. http://dx.doi.org/10.1093/gerona/gly261.

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Abstract Understanding the effect of molecular pathways involved in the age-dependent deterioration of stem cell function is critical for developing new therapies. The overexpression of Klotho (KL), an antiaging protein, causes treated animal models to enjoy extended life spans. Now, the question stands: Does KL deficiency accelerate stem cell aging and telomere shortening? If so, what are the specific mechanisms by which it does this, and is cycloastragenol (CAG) treatment enough to restore telomerase activity in aged stem cells? We found that KL deficiency diminished telomerase activity by a

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Tomlinson, Rebecca L., Tania D. Ziegler, Teerawit Supakorndej, Rebecca M. Terns, and Michael P. Terns. "Cell Cycle-regulated Trafficking of Human Telomerase to Telomeres." Molecular Biology of the Cell 17, no. 2 (2006): 955–65. http://dx.doi.org/10.1091/mbc.e05-09-0903.

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Telomerase synthesizes telomeres at the ends of human chromosomes during S phase. The results presented here suggest that telomerase activity may be regulated by intranuclear trafficking of the key components of the enzyme in human cells. We examined the subcellular localization of endogenous human telomerase RNA (hTR) and telomerase reverse transcriptase (hTERT) in HeLa cervical carcinoma cells. Throughout most of the cell cycle, we found that the two essential components of telomerase accumulate at intranuclear sites separate from telomeres. However, during S phase, both hTR and hTERT are sp

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Brailova, Natalia Vasil'evna, Ekaterina Nail'evna Dudinskaya, Olga Nikolaevna Tkacheva, et al. "Telomere length, telomerase activity and mechanisms change in patients with type 2 diabetes mellitus." Problems of Endocrinology 62, no. 1 (2016): 16–24. http://dx.doi.org/10.14341/probl201662116-24.

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Aim.To study the association of chronic inflammation, oxidative stress with telomere biology in people with type 2 diabetes mellitus (T2DM).Material and Methods.A total 50 patients with T2D and without cardiovascular disease (CVD) and 139 people from control group were included in the study. All subjects were measured for carbohydrate metabolism; oxidative stress (malondialdehyde (MDA)); inflammation (C-reactive protein — CRP, fibrinogen, interleukin-6); lymphocyte telomere length, telomerase activity.Results.In diabetic patients telomeres were shorter than in controls (9.59±0.54 and 9.76±0.47

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Schaetzlein, S., and K. L. Rudolph. "Telomere length regulation during cloning, embryogenesis and ageing." Reproduction, Fertility and Development 17, no. 2 (2005): 85. http://dx.doi.org/10.1071/rd04112.

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Telomeres are nucleoprotein complexes at the end of eukaryotic chromosomes with an essential role in chromosome capping. Owing to the end-replication problem of DNA polymerase, telomeres shorten during each cell division. When telomeres become critically short, they loose their capping function, which in turn induces a DNA damage-like response. This mechanism inhibits cell proliferation at the senescence stage and there is evidence that it limits the regenerative capacity of tissues and organs during chronic diseases and ageing. The holoenzyme telomerase synthesises telomeric DNA de novo, but,

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Marques, Francine Z., Scott A. Booth, Priscilla R. Prestes, et al. "Telomere dynamics during aging in polygenic left ventricular hypertrophy." Physiological Genomics 48, no. 1 (2016): 42–49. http://dx.doi.org/10.1152/physiolgenomics.00083.2015.

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Short telomeres are associated with increased risk of cardiovascular disease. Here we studied cardiomyocyte telomere length at key ages during the ontogeny of cardiac hypertrophy and failure in the hypertrophic heart rat (HHR) and compared these with the normal heart rat (NHR) control strain. Key ages corresponded with the pathophysiological sequence beginning with fewer cardiomyocytes (2 days), leading to left ventricular hypertrophy (LVH) (13 wk) and subsequently progression to heart failure (38 wk). We measured telomere length, tissue activity of telomerase, mRNA levels of telomerase revers

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Meier, Bettina, Lucia Driller, Sigrun Jaklin, and Heidi M. Feldmann. "New Function of CDC13 in Positive Telomere Length Regulation." Molecular and Cellular Biology 21, no. 13 (2001): 4233–45. http://dx.doi.org/10.1128/mcb.21.13.4233-4245.2001.

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ABSTRACT Two roles for the Saccharomyces cerevisiae Cdc13 protein at the telomere have previously been characterized: it recruits telomerase to the telomere and protects chromosome ends from degradation. In a synthetic lethality screen with YKU70, the 70-kDa subunit of the telomere-associated Yku heterodimer, we identified a new mutation in CDC13, cdc13-4, that points toward an additional regulatory function of CDC13. AlthoughCDC13 is an essential telomerase component in vivo, no replicative senescence can be observed in cdc13-4 cells. Telomeres of cdc13-4 mutants shorten for about 150 generat

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Calado, Rodrigo T., William T. Yewdell, Keisha L. Wilkerson, Joshua A. Regal, Sachiko Kajigaya, and Neal S. Young. "Sex Hormones Modulate the Length of Telomeres of Normal and Telomerase-Mutant Leukocytes through the Estrogen Receptor Pathway." Blood 108, no. 11 (2006): 182. http://dx.doi.org/10.1182/blood.v108.11.182.182.

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Abstract Telomeres are nucleoprotein complexes at chromosome ends that protect chromosomes from end-to-end fusion, damage, and recombination. Telomeres are eroded during cell division due to DNA polymerase’s inability to fully duplicate them. Immature cells, including hematopoietic stem cells, express telomerase to maintain telomere lengths. Mutations in genes encoding the telomerase complex (TERT, coding for the reverse transcriptase, and TERC, coding for the RNA component) are associated with constitutional and acquired aplastic anemia, causing low telomerase activity, short telomeres, and a

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Smogorzewska, Agata, Bas van Steensel, Alessandro Bianchi, et al. "Control of Human Telomere Length by TRF1 and TRF2." Molecular and Cellular Biology 20, no. 5 (2000): 1659–68. http://dx.doi.org/10.1128/mcb.20.5.1659-1668.2000.

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ABSTRACT Telomere length in human cells is controlled by a homeostasis mechanism that involves telomerase and the negative regulator of telomere length, TRF1 (TTAGGG repeat binding factor 1). Here we report that TRF2, a TRF1-related protein previously implicated in protection of chromosome ends, is a second negative regulator of telomere length. Overexpression of TRF2 results in the progressive shortening of telomere length, similar to the phenotype observed with TRF1. However, while induction of TRF1 could be maintained over more than 300 population doublings and resulted in stable, short tel

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Calado, Rodrigo T., and Neal S. Young. "Telomere maintenance and human bone marrow failure." Blood 111, no. 9 (2008): 4446–55. http://dx.doi.org/10.1182/blood-2007-08-019729.

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AbstractAcquired and congenital aplastic anemias recently have been linked molecularly and pathophysiologically by abnormal telomere maintenance. Telomeres are repeated nucleotide sequences that cap the ends of chromosomes and protect them from damage. Telomeres are eroded with cell division, but in hematopoietic stem cells, maintenance of their length is mediated by telomerase. Accelerated telomere shortening is virtually universal in dyskeratosis congenita, caused by mutations in genes encoding components of telomerase or telomere-binding protein (TERT, TERC, DKC1, NOP10, or TINF2). About on

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Broccoli, D., L. A. Godley, L. A. Donehower, H. E. Varmus, and T. de Lange. "Telomerase activation in mouse mammary tumors: lack of detectable telomere shortening and evidence for regulation of telomerase RNA with cell proliferation." Molecular and Cellular Biology 16, no. 7 (1996): 3765–72. http://dx.doi.org/10.1128/mcb.16.7.3765.

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Activation of telomerase in human cancers is thought to be necessary to overcome the progressive loss of telomeric DNA that accompanies proliferation of normal somatic cells. According to this model, telomerase provides a growth advantage to cells in which extensive terminal sequence loss threatens viability. To test these ideas, we have examined telomere dynamics and telomerase activation during mammary tumorigenesis in mice carrying a mouse mammary tumor virus long terminal repeat-driven Wnt-1 transgene. We also analyzed Wnt-1-induced mammary tumors in mice lacking p53 function. Normal mamma

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Halvorsen, Tanya L., Gil Leibowitz, and Fred Levine. "Telomerase Activity Is Sufficient To Allow Transformed Cells To Escape from Crisis." Molecular and Cellular Biology 19, no. 3 (1999): 1864–70. http://dx.doi.org/10.1128/mcb.19.3.1864.

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ABSTRACT The introduction of simian virus 40 large T antigen (SVLT) into human primary cells enables them to proliferate beyond their normal replicative life span. In most cases, this temporary escape from senescence eventually ends in a second proliferative block known as “crisis,” during which the cells cease growing or die. Rare immortalization events in which cells escape crisis are frequently correlated with the presence of telomerase activity. We tested the hypothesis that telomerase activation is the critical step in the immortalization process by studying the effects of telomerase acti

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Damle, Rajendra N., Taraneh Banapour, Cristina Sison, Steven L. Allen, Kanti R. Rai, and Nicholas Chiorazzi. "Evidence for Alternative Lengthening of Telomeres in Chronic Lymphocytic Leukemia Patients." Blood 106, no. 11 (2005): 1179. http://dx.doi.org/10.1182/blood.v106.11.1179.1179.

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Abstract Telomere shortening is a consequence of repetitive clonal replication and leads to clonal deletion unless DNA extension and repair occur. All tumors must circumvent this problem by up-regulating mechanisms that lead to chromosomal lengthening. Two mechanisms have been identified that maintain chromosome ends- telomerase that does so by reverse transcription and alternative lengthening of telomeres (ALT) that occurs by homologous recombination. The latter function is characterized by the presence of promyelocytic leukemia protein-associated nuclear bodies (PML-NBs) and the presence of

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Auchter, Morgan, Sandrine Medves, Laetitia Chambeau, et al. "Mechanisms of Telomere Maintenance Dysfunction in B-Chronic Lymphocytic Leukemia Through CpG Island Methylation." Blood 120, no. 21 (2012): 3489. http://dx.doi.org/10.1182/blood.v120.21.3489.3489.

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Abstract Abstract 3489 Telomeres are a repetitive DNA sequences associated with a protein complex named shelterin that protect chromosome ends. Two types of mechanisms maintain telomere in cancer cells. The first involves telomerase an enzyme able to copy the telomeric motif that consists of three principal subunits, including the telomerase reverse transcriptase hTERT. The second, named ALT (Alternative Lengthening of Telomere), corresponds to the recombination between telomeres that involves notably a complex formed by the topoisomerase III alpha (hTopoIIIa), BLM, RMI1 and RMI2. Little is kn

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