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Telomere Length Dynamics and Chromosomal Instability in Cells Derived from Telomerase Null Mice
Open accessAbstract
To study the effect of continued telomere shortening on chromosome stability, we have analyzed the telomere length of two individual chromosomes (chromosomes 2 and 11) in fibroblasts derived from wild-type mice and from mice lacking the mouse telomerase RNA (mTER) gene using quantitative fluorescence in situ hybridization. Telomere length at both chromosomes decreased with increasing generations of mTER−/− mice. At the 6th mouse generation, this telomere shortening resulted in significantly shorter chromosome 2 telomeres than the average telomere length of all chromosomes. Interestingly, the most frequent fusions found in mTER−/− cells were homologous fusions involving chromosome 2. Immortal cultures derived from the primary mTER−/− cells showed a dramatic accumulation of fusions and translocations, revealing that continued growth in the absence of telomerase is a potent inducer of chromosomal instability. Chromosomes 2 and 11 were frequently involved in these abnormalities suggesting that, in the absence of telomerase, chromosomal instability is determined in part by chromosome-specific telomere length. At various points during the growth of the immortal mTER−/− cells, telomere length was stabilized in a chromosome-specific man-ner. This telomere-maintenance in the absence of telomerase could provide the basis for the ability of mTER−/− cells to grow indefinitely and form tumors.
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“In the G5-G6 TERCÀ/À tissues, there was clear cytogenetic evidence of progressive telomere erosion including 'signal-free' ends, chromosomal end-to-end fusions and anaphase bridging at mitosis (60)(61)(62).”
From Telomeres and telomerase in cancer (2010) · cites this paper as [61]
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“G5-G6 TERC mice became infertile, showed high rates of apoptosis in testis and germ cell depletion, exhibited impaired bone marrow function and diminished proliferation of lymphocytes (61).”
From Telomeres and telomerase in cancer (2010) · cites this paper as [61]
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“Indeed, continued breeding of first generation (G1) TERCÀ/À mice to yield successive generations of TERCÀ/À mice resulted in progressive loss of telomere reserves and ultimately provoked severe degeneration of highly proliferative tissues.”
From Telomeres and telomerase in cancer (2010) · cites this paper as [61]
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Cites
Telomeres shorten during ageing of human fibroblasts
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“Indeed, telomere shortening to a critical length has been proposed to limit the life span of somatic cells in humans (Harley et al., 1990; Counter et al., 1992).”
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Bodnar, A. G., Ouellette, M., Frolkis, M., Holt, S. E., Chiu, C.-P., Morin, G. B., Harley, C. B., Shay, J. W., Lichtsteiner, S., & Wright, W. E. (1998) · Science · doi:10.1126/science.279.5349.349 · Cited by 4,975 · cited 2×
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Items 201–300 of 313
Gopalakrishnan, K., Low, G. K. M., Ting, A. P. L., Srikanth, P., Slijepčević, P., & Hande, M. P. (2010) · Genome Integrity · doi:10.1186/2041-9414-1-16 · Cited by 29
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Self-citationTelomere dynamics in Fancg-deficient mouse and human cells
Franco, S., van de Vrugt, H. J., Fernández, P., Aracil, M., Arwert, F., & Blasco, M. A. (2004) · Blood · doi:10.1182/blood-2003-10-3626 · Cited by 30
Self-citationBorghini, A., Roursgaard, M., Andreassi, M. G., Kermanizadeh, A., & Möller, P. (2016) · Mutagenesis · doi:10.1093/mutage/gew036 · Cited by 28
“The high number of guanine residues in telomeric DNA sequences increases the probability of the accumulation of 8-oxodG in telomeres during oxidative stress, which may lead to accelerated telomere shortening (31, 32).”
BackgroundLow, G. K. M., Fok, E. D. Z., Ting, A. P. L., & Hande, M. P. (2008) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2008.05.009 · Cited by 27
Self-citationTelomeric recombination induced by dysfunctional telomeres
Brault, M. E., & Autexier, C. (2010) · Molecular Biology of the Cell · doi:10.1091/mbc.e10-02-0173 · Cited by 28
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BackgroundTelomere Biology—Insights into an Intriguing Phenomenon
Venkatesan, S., Khaw, A. K., & Hande, M. P. (2017) · Cells · doi:10.3390/cells6020015 · Cited by 29
Self-citationGenomic Biomarkers to Improve Ulcerative Colitis Neoplasia Surveillance
Bronner, M. P., O'Sullivan, J. N., Rabinovitch, P. S., Crispin, D. A., Chen, L., Emond, M. J., Rubin, C. E., & Brentnall, T. A. (2008) · American Journal Of Pathology · doi:10.2353/ajpath.2008.080250 · Cited by 27
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Self-citationIs telomere erosion a mechanism of species extinction?
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BackgroundLow temperature tolerance of human embryonic stem cells
Heng, B. C., Vinoth, K. J., Liu, H., Hande, M. P., & Cao, T. (2006) · International Journal of Medical Sciences · doi:10.7150/ijms.3.124 · Cited by 24
“The chromosomes of hESC upon exposure to low temperature (25oC and 4oC for 24 h and 48 h) was analyzed by fluorescence in situ hybridization (FISH) of metaphase spreads (Figure 2A to E) with telomere and centromere-specific peptide nucleic acid (PNA) probes [5].”
Self-citationTelomeres and telomerase in T cells of tumor immunity
Qian, Y., Yang, L., & Cao, S. (2014) · Cellular Immunology · doi:10.1016/j.cellimm.2014.03.009 · Cited by 23
“recognized by DNA-damage responses that can lead to chromosomal fusions and/or chromosomal instability and serve as a primer for the replication of DNA ends during cell division [12].”
BackgroundTcstv1 and Tcstv3 elongate telomeres of mouse ES cells
Zhang, Q., Dan, J., Wang, H., Guo, R., Mao, J., Fu, H., Wei, X., & Liu, L. (2016) · Scientific Reports · doi:10.1038/srep19852 · Cited by 24
Vinoth, K. J., Heng, B. C., Poonepalli, A., Banerjee, B., Balakrishnan, L., Lü, K., Hande, M. P., & Cao, T. (2008) · Stem Cells and Development · doi:10.1089/scd.2007.0088 · Cited by 23
“Peptide nucleic acid fluorescence in situ hybridization (PNA-FISH) [20] was used to evaluate chromosomal aberrations, whereas multicolor (m) FISH [21] allowed further elucidation of the specific type of chromosomal aberration incurred upon exposure to MMC.”
Self-citationGan, Y., Mo, Y., Johnston, J. S., Lu, J. L., Wientjes, M. G., & Au, J. L. ‐. (2002) · FEBS Letters · doi:10.1016/s0014-5793(02)03141-1 · Cited by 24
Telomere-Mediated Chromosomal Instability Triggers TLR4 Induced Inflammation and Death in Mice
Bhattacharjee, R. N., Banerjee, B., Akira, S., & Hande, M. P. (2010) · PLoS ONE · doi:10.1371/journal.pone.0011873 · Cited by 22
“FISH with Cy-3 labelled (CCCTAA)3 peptide nucleic acid, and subsequent quantitative analysis of digital images were performed [6].”
InfluentialSelf-citationTahara, T., Shibata, T., Okubo, M., Kawamura, T., Sumi, K., Ishizuka, T., Nakamura, M., Nagasaka, M., Nakagawa, Y., Ohmiya, N., et al. (2014) · Clinical and Experimental Medicine · doi:10.1007/s10238-014-0295-4 · Cited by 22
Zou, Y. S., Tong, H. J., Li, M., Tan, K. S., & Cao, T. (2016) · Biogerontology · doi:10.1007/s10522-016-9662-8 · Cited by 22
“When telomere shortens to a critical length, decrease in cell proliferation or replicative senescence is triggered in these cells (Allsopp et al. 1992; Counter et al. 1992; Hande et al. 1999; Wright et al. 1989).”
BackgroundMaida, Y., Kyo, S., Forsyth, N., Takakura, M., Sakaguchi, J., Mizumoto, Y., Hashimoto, M., Nakamura, M., Nakao, S., & Inoue, M. (2006) · The Journal of Pathology · doi:10.1002/path.2038 · Cited by 21
“These observations support the theory, established using mouse models, that telomere instability causes cancer initiation and that subsequent telomerase activation and late-stage stabilization of telomeres are required for malignant progression of cells [7,21].”
BackgroundTahara, T., Shibata, T., Kawamura, T., Ishizuka, T., Okubo, M., Nagasaka, M., Nakagawa, Y., Arisawa, T., Ohmiya, N., & Hirata, I. (2015) · Clinical and Experimental Medicine · doi:10.1007/s10238-014-0335-0 · Cited by 20
Chromosomal instability: a key driver in glioma pathogenesis and progression
Mazzoleni, A., Awuah, W. A., Sanker, V., Bharadwaj, H. R., Aderinto, N., Tan, J. K., Huang, H. Y. R., Poornaselvan, J., Shah, M. H., Atallah, O., et al. (2024) · European journal of medical research · doi:10.1186/s40001-024-02043-8 · Cited by 21
“Critical telomere shortening leads to telomere malfunction, followed by successive bridge-fusion-breakage cycles, and results in numerical chromosomal abnormalities [39, 40].”
BackgroundTelomere Maintenance as Therapeutic Target in Embryonal Tumours
Shalaby, T., Hiyama, E., & Grotzer, M. A. (2010) · Anti-Cancer Agents in Medicinal Chemistry · doi:10.2174/1871520611009030196 · Cited by 20
“In this scenario, as telomeres shorten with each cell cycle the "sticky" ends of chromosomes become prone to fusions [85], leading to subsequent chromosomal instability [86-88] and offering a mechanism for a continuous rearrangement of chromosome structure that might contribute to oncogene amplification and tumour sup…”
BackgroundEpigenetic Regulation of Telomere Chromatin Integrity in Pluripotent Embryonic Stem Cells
Wong, L. H. (2010) · Epigenomics · doi:10.2217/epi.10.49 · Cited by 23
How Cells Handle DNA Breaks during Mitosis: Detection, Signaling, Repair, and Fate Choice
Thompson, R. H., Gatenby, R., & Sidi, S. (2019) · Cells · doi:10.3390/cells8091049 · Cited by 19
“In addition to DNA breaks, these chromatin bridges can be formed by consistent chromatid cohesion [27] and by telomere shortening [28].”
BackgroundRadiation-induced chromosome breaks in ataxia-telangiectasia cells remain open
Martı́n, M., Genescà, A., Latre, L., Ribas, M., Miró, R., Egozcue, J., & Tusell, L. (2003) · International Journal of Radiation Biology · doi:10.1080/0955300031000089601 · Cited by 19
“…with many reports that It has been presumed that the de novo formation of telomeres by telomerase could only occur in cells thatrepeatedly show A-T cells to be hypersensitive to IR exposure (Mozdarani and Bryant 1989, Pandita and have difficulties in rejoining the ends of DSBs (Sprung et al. 1999).”
BackgroundInfluentialTelomerase: Not Just Black and White, but Shades of Gray
Liu, J. (2000) · Molecular Cell Biology Research Communications · doi:10.1006/mcbr.2000.0203 · Cited by 18
Biochemical properties of Trypanosoma cruzi telomerase
Muñoz, D. P. (2004) · Nucleic Acids Research · doi:10.1093/nar/gkh864 · Cited by 18
“The ALT pathway can efficiently immortalize cultured mouse fibroblasts (23), but mice themselves cannot remain healthy and reproduce without telomerase enzyme for more than a few generations (19).”
BackgroundGeorge, A., Venkatesan, S., Ashok, N., Saraswathy, R., & Hande, M. P. (2018) · Mutation Research/Genetic Toxicology and Environmental Mutagenesis · doi:10.1016/j.mrgentox.2018.06.015 · Cited by 18
Self-citationTing, A. P. L., Low, G. K. M., Gopalakrishnan, K., & Hande, M. P. (2009) · Journal of Cellular and Molecular Medicine · doi:10.1111/j.1582-4934.2009.00945.x · Cited by 18
“Telomeres cap chromosomal ends and are important for chromosome integrity and segregation [29, 42].”
BackgroundInfluentialSelf-citationGupta, N., Taneja, R., Pandey, A., Mukesh, M., Singh, H., & Gupta, S. C. D. (2007) · Cell Biology International · doi:10.1016/j.cellbi.2007.05.004 · Cited by 18
“The clonal differences due to increased passage number may be attributed to chromosomal instability associated with telomere shortening and perhaps also to mitotic recombination (Hande et al., 1999).”
BackgroundPark, J.-E., Woo, S. R., Kang, C.-M., Juhn, K.-M., Ju, Y.-J., Shin, H.-J., Joo, H.-Y., Park, E. R., Park, I.-C., Hong, S. H., et al. (2010) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2010.12.018 · Cited by 17
Telomeres and telomerase in adrenocortical tissue maintenance, carcinogenesis, and aging
Else, T. (2009) · Journal of Molecular Endocrinology · doi:10.1677/jme-08-0189 · Cited by 17
“…chromosomes have been found in telomerase-deficient cells as well as in MEFs from Pot1-deficient animals and from adrenocortical dysplasia (acd)mice, whichharbor amutation in theTpp1/Acd gene (Hande et al. 1999, He et al. 2006, Hockemeyer et al. 2006, 2007, Wu et al. 2006, Else et al. 2007).”
BackgroundBeauchamp‐Nicoud, A., Feneux, D., Bayle, C., Bernheim, A., Léonard, C., Koscielny, S., Tchernia, G., & Bourhis, J. (2003) · British Journal of Haematology · doi:10.1046/j.1365-2141.2003.04388.x · Cited by 17
“This has been suggested to generate increased chromosome instability, which in turn leads to increased telomerase activity and/or other mechanisms aimed at maintaining telomere length, potentially leading to the immortalization of mutated cells (Hande et al, 1999).”
BackgroundVu, T., Davidson, S.-L., Borgesi, J., Mowla, M., Jeon, T., & Shim, J. (2017) · RSC Advances · doi:10.1039/c7ra08063h · Cited by 18
Argilla, D., Chin, K., Singh, M., Hodgson, J. G., Bosenberg, M., Ortíz-de-Solórzano, C., Lockett, S. J., DePinho, R. A., Gray, J. W., & Hanahan, D. (2004) · Cancer Cell · doi:10.1016/j.ccr.2004.08.032 · Cited by 16
Gurung, R. L., Balakrishnan, L., Bhattacharjee, R. N., Manikandan, J., Swaminathan, S., & Hande, M. P. (2010) · Genome Integrity · doi:10.1186/2041-9414-1-5 · Cited by 16
“Fluorescence in situ hybridisation (FISH) was performed using telomere specific PNA probe labelled with Cy3 and the cells were counterstained with 4’, 6-Diamidino-2-phenylindole (DAPI, Vectashield) [11].”
BackgroundMethodSelf-citationGopalakrishnan, K., Venkatesan, S., Low, E. S. H., & Hande, M. P. (2018) · Mutation Research/Genetic Toxicology and Environmental Mutagenesis · doi:10.1016/j.mrgentox.2018.03.008 · Cited by 15
Self-citationGenomic instability demonstrates similarity between DCIS and invasive carcinomas
Heaphy, C. M., Bisoffi, M., Joste, N. E., Baumgartner, K. B., Baumgartner, R., & Griffith, J. K. (2008) · Breast Cancer Research and Treatment · doi:10.1007/s10549-008-0165-4 · Cited by 15
“Telomeres are located at and stabilize the ends of eukaryotic chromosomes, thus preventing degradation and recombination [11–13].”
BackgroundFinnon, P., Wong, H.-P., Silver, A. R., Slijepčević, P., & Bouffler, S. D. (2001) · International Journal of Radiation Biology · doi:10.1080/09553000110075220 · Cited by 15
“This is consisttankyrase have been shown to have a role in telomer-ent with the ndings of Hande et al. (1999) who ase regulation (Wang et al. 1998, Wu et al. 1999,showed that the majority of RLF from late passage Smith and de Lange, 2000) .”
BackgroundExtensive cytogenetic heterogeneity in a benign retroperitoneal schwannoma
Gorunova, L., Dawiskiba, S., Andrén‐Sandberg, Å., Höglund, M., & Johansson, B. (2001) · Cancer Genetics and Cytogenetics · doi:10.1016/s0165-4608(00)00440-4 · Cited by 15
Bojović, B., & Crowe, D. L. (2011) · Molecular Carcinogenesis · doi:10.1002/mc.21834 · Cited by 13
“telomeres show accumulation of chromosomal fusions and translocations because of end fusions and anaphase breaks [27].”
BackgroundWen, V. W., Wu, K., Baksh, S., Hinshelwood, R. A., Lock, R. B., Clark, S. J., Moore, M. A. S., & MacKenzie, K. L. (2006) · Cancer Research · doi:10.1158/0008-5472.can-06-0979 · Cited by 13
Lack of association between PBMC telomere length and endurance exercise
Denham, J. (2016) · Journal of Applied Biomedicine · doi:10.1016/j.jab.2016.09.004 · Cited by 14
Evaluation of telomere length in human cardiac tissues using cardiac quantitative FISH
Sharifi‐Sanjani, M., Meeker, A. K., & Mourkioti, F. (2017) · Nature Protocols · doi:10.1038/nprot.2017.082 · Cited by 13
On BLM helicase in recombination-mediated telomere maintenance
Rezazadeh, S. (2012) · Molecular Biology Reports · doi:10.1007/s11033-012-2379-0 · Cited by 15
Peitl, P. (2002) · Mutagenesis · doi:10.1093/mutage/17.1.67 · Cited by 13
Repair of DNA Broken Ends is Similar in Embryonic Fibroblasts with and without Telomerase
Latre, L., Genescà, A., Martı́n, M., Ribas, M., Egozcue, J., Blasco, M. A., & Tusell, L. (2004) · Radiation Research · doi:10.1667/rr3203 · Cited by 12
Self-citationMehdipour, P., Kheirollahi, M., Mehrazin, M., Kamalian, N., & Atri, M. (2011) · Cell Biology International · doi:10.1042/cbi20100560 · Cited by 11
“However, alteration of TL and proliferative potential could be referred to in studies conducted in vitro or in mice (Harley et al., 1992; Levy et al., 1992; Allsopp and Harley, 1995; Blasco et al., 1997; Hande et al., 1999; Wan et al., 1999).”
BackgroundTerminal regions of mammal chromosomes: Plasticity and role in evolution
Zhdanova, N. S., Рубцов, Н. Б., & Minina, Y. M. (2007) · Russian Journal of Genetics · doi:10.1134/s1022795407070022 · Cited by 11
Irie, H., Yamamoto, I., Tarumoto, Y., Tashiro, S., Runge, K. W., & Ishikawa, F. (2019) · PLoS Genetics · doi:10.1371/journal.pgen.1008335 · Cited by 11
“Previous studies have pointed to the requirement of chromosome maintenance mechanisms for suppression of GCRs, including DNA repair and telomere protection pathways [2, 3].”
BackgroundPotential clinical role of telomere length in human glioblastoma.
Torre, D. L., Aguennouz, M., Conti, A., Giusa, M., Raffa, G., Abbritti, R. V., Germanò, A., & Angileri, F. F. (2011) · Europe PMC (PubMed Central) · Cited by 10
Castori, M., Ceccarini, C., Castiglia, D., Ruggeri, S., Dallapiccola, B., & Zambruno, G. (2007) · British Journal of Dermatology · doi:10.1111/j.1365-2133.2006.07661.x · Cited by 10
Genomic instability in�both wild-type and telomerase null MEFs
Hao, L.-Y., & Greider, C. W. (2004) · Chromosoma · doi:10.1007/s00412-004-0291-7 · Cited by 9
“When mouse embryonic fibroblast (MEF) lines from late generation mTR−/− mouse are grown in culture, they immortalize and grow as rapidly as wild-type MEFs, suggesting they maintain telomeres via an alternative mechanism (Blasco et al. 1997; Hande et al. 1999).”
BackgroundFossel, M. (2003) · Rejuvenation Research · doi:10.1089/109454503769684793 · Cited by 9
“210 In such (mTR 2 / 2 ) mice, telomere lengths fall with each successive generation, 211 but even in the earliest generation we find defects in neural tube closure, 212 as well as in highly proliferative tissues, affecting spermatogenesis, hematopoesis, etc. 213 As discussed previously,…”
Replicative Senescence and Cancer
Hornsby, P. J. (2006) · Kluwer Academic Publishers eBooks · doi:10.1007/0-387-23962-6_3 · Cited by 9
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Blasco, M. A. (2001) · BioMed Research International · doi:10.1155/s1110724301000109 · Cited by 8
“Such telomere maintenance mechanisms seem to be selected when telomeres reach a critical short length, chromosomal abnormalities have occurred and cell viability has been compromised [9].”
BackgroundSelf-citationGenetics of Beckwith‐Wiedemann syndrome‐associated tumors: Common genetic pathways
Steenman, M., Westerveld, A., & Mannens, M. M. A. M. (2000) · Genes Chromosomes and Cancer · doi:10.1002/(sici)1098-2264(200005)28:1 · Cited by 105
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RAD51 separation of function mutation disables replication fork maintenance but preserves DSB repair
Son, M. Y., Beláň, O., Špı́rek, M., Cibulka, J., Nikulenkov, F., Kim, Y. Y., Hwang, S., Myung, K., Montagna, C., Kim, T. M., et al. (2024) · iScience · doi:10.1016/j.isci.2024.109524 · Cited by 5
Télomères : un Nobel pour le début de la fin
Rajpar, S., Guittat, L., & Mergny, J. (2011) · Bulletin du Cancer · doi:10.1684/bdc.2011.1378 · Cited by 9
Inhibition of gene amplification in telomerase deficient immortalized mouse embryonic fibroblasts
Rebuzzini, P., Martinelli, P., Blasco, M. A., Giulotto, E., & Mondello, C. (2006) · Carcinogenesis · doi:10.1093/carcin/bgl158 · Cited by 7
Self-citationRad54 is dispensable for the ALT pathway
Akiyama, K., Yusa, K., Hashimoto, H., Poonepalli, A., Hande, M. P., Kakazu, N., Takeda, J., Tachibana, M., & Shinkai, Y. (2006) · Genes to Cells · doi:10.1111/j.1365-2443.2006.01020.x · Cited by 8
“1308 To further analyze the telomere dynamics in Rad54deficient D107A9Cre, we performed cytogenetic analysis of metaphase spread chromosomes by quantitative fluorescence in situ hybridization (Q-FISH) with the (C3TA2)3 PNA probe (Zijlmans et al. 1997; Hande et al. 1999).”
MethodSelf-citationIs DNA Damage Response Ready for Action Anywhere?
Terradas, M., Martı́n, M., Hernández, L., Tusell, L., & Genescà, A. (2012) · International Journal of Molecular Sciences · doi:10.3390/ijms130911569 · Cited by 7
“unprotected ends resulting from telomeric dysfunction [2,3], or by the fusion of an unprotected end and a broken chromosome [4].”
BackgroundIn vitro aging of rat lung cells
Petitot, F., Lebeau, J., Dano, L., Lectard, B., Altmeyer, S., Levalois, C., & Chevillard, S. (2003) · Experimental Cell Research · doi:10.1016/s0014-4827(03)00103-4 · Cited by 7
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“Additionally, they are believed to prevent broken chromosomes from rearranging and fusing and are involved in chromosome segregation [16–18].”
BackgroundSanpedro-Luna, J. A., Jacinto-Vázquez, J. J., Anastacio-Marcelino, E., Posadas-Gutiérrez, C. M., Olmos-Pineda, I., González-Bernal, J. A., Carcaño-Montiel, M. G., Vega‐Alvarado, L., Vázquez‐Cruz, C., & Alonso, P. S. (2023) · PLoS ONE · doi:10.1371/journal.pone.0281251 · Cited by 6
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“In mice, one of the consequences of impaired telomere function is a form of genomic instability characterized by a high frequency of Robertsonianlike fusions between chromosomes (Blasco et al. 1997, Lee et al. 1998, Hande et al. 1999).”
BackgroundBasidiomycetes Telomeres – A Bioinformatics Approach
Ramı́rez, L., Pérez, G., Castanera, R., Santoyo, F., & Antonio, G. (2011) · InTech eBooks · doi:10.5772/21620 · Cited by 5
“They are usually found in repair- and/or telomerase-deficient cells (Bailey et al., 1999; Blasco et al., 1997; Hande, 2004; Hande et al., 1999; Lo et al., 2002; Samper et al., 2000) with a variety of mutations affecting telomere function, including those occurring in proteins of the”
BackgroundNon-Disruptive PNAFISH Protocol for Formalin-Fixed and Paraffin-Embedded Tissue Sections
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BackgroundTelomere and Telomerase for the Regulation of Stem Cells
Hiyama, E., & Hiyama, K. (2009) · Humana Press eBooks · doi:10.1007/978-1-60327-227-8_11 · Cited by 4
“ALT mechanisms are also activated in Terc-deficient mice in cultured mouse embryonic fibroblasts and embryonic stem cells [31–33], and in vivo during germinal center formation [34], which indicates that ALT mechanisms can also be selected in nontumoral settings.”
BackgroundThe Role of Telomeres in Liver Disease
Sunami, Y., von Figura, G., Kleger, A., Strnad, P., Hüser, N., & Hartmann, D. (2014) · Progress in molecular biology and translational science · doi:10.1016/b978-0-12-397898-1.00007-4 · Cited by 5
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BackgroundCozzolino, M., Ergun, Y., Ristori, E., Garg, A., Imamoglu, G., & Seli, E. U. (2024) · Aging · doi:10.18632/aging.205543 · Cited by 2
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BackgroundTelomere--the twilight to immortality.
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Genomic Instability and DNA Repair
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Telomere as an Important Player in Regulation of Microbial Pathogen Virulence
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Metadata
- Authors
- Hande, M. P., Samper, E., Lansdorp, P., & Blasco, M. A.
- Affiliations
- University of British Columbia (CA)
- *Department of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC, Campus Cantoblanco, Madrid E-28049, Spain; ‡Terry Fox Laboratory, British Columbia Cancer Research Center, Vancouver, British Columbia V5Z 1L3, Canada; and §Department of Medicine, University of British Columbia, Vancouver, British Columbia V6T 2B5, Canada
- Venue
- The Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 1999-02-22
- Volume
- 144
- Issue
- 4
- Pages
- 589-601
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- PMC
- PMC2132934
- OpenAlex
- W2110286112
- Cited by
- 313
- References
- 63
- Citations by year
- 2026: 1 · 2024: 5 · 2023: 1 · 2020: 1 · 2019: 6 · 2018: 7 · 2017: 5 · 2016: 10 · 2015: 8 · 2014: 8 · 2013: 10 · 2012: 7
- FWCI
- 16.53
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- cc-by-nc-sa
- Locations
- The Journal of Cell Biology (publishedVersion)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (1r01gm056162-01)
- National Cancer Institute (P01CA013106)
- National Institute of General Medical Sciences (GM56162)
- National Institute of Allergy and Infectious Diseases (R01AI029524)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Chromosomal and Genetic Variations
- Keywords
- telomere length, chromosomal instability, telomerase RNA, telomere shortening, chromosome 2, chromosome 11, translocation, cell immortalization, fibroblasts, tumor formation, telomere maintenance
- MeSH terms
- Animals, Cell Transformation, Neoplastic, Cells, Cultured, Chromosome Aberrations, Models, Genetic, Neoplasms, Experimental, Telomere, In Situ Hybridization, Fluorescence, Mice, Knockout, Telomerase, Mice
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