The DOI matches its Crossref record; 40 of the 40 references it cites were found in a registry or an index.
Essential role of mouse telomerase in highly proliferative organs
Abstract
We have investigated the role of the enzyme telomerase in highly proliferative organs in successive generations of mice lacking telomerase RNA. Late-generation animals exhibited defective spermatogenesis, with increased programmed cell death (apoptosis) and decreased proliferation in the testis. The proliferative capacity of haematopoietic cells in the bone marrow and spleen was also compromised. These progressively adverse effects coincided with substantial erosion of telomeres (the termini of eukaryotic chromosomes) and fusion and loss of chromosomes. These findings indicate an essential role for telomerase, and hence telomeres, in the maintenance of genomic integrity and in the long-term viability of high-renewal organ systems.
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In the citing paper
“Similarly, in the testes, we observed the previously reported testicular atrophy and associated apoptotic depletion of germ cells in late-generation mTerc -/ -mice (32), with comparable reduction in testes weights ( P = 0.4131) and depletion of germ cells in all three Ink4a / Arf genotypes (Fig. 1 E ).”
From Ink4a / Arf tumor suppressor does not modulate the degenerative conditions or tumor spectrum of the telomerase-deficient mouse (2007) · cites this paper as [32]
In the citing paper
“Telomerase knock-out (mTERC−/−) mice which carry a homozygous deletion of the RNA component of telomerase (Blasco et al., 1997) show a generation-dependent telomere shortening, which results in critically short telomeres and both senescence and apoptosis (Lee et al., 1998).”
From Telomeres and cell senescence—size matters not (2017) · cites this paper as Lee et al., 1998
In the citing paper
“In the absence of telomerase, continued cell division results in telomere shortening, loss of ‘capping’ function, and p53 activation12-15.”
From Telomere dysfunction induces metabolic and mitochondrial compromise (2011) · cites this paper as [13]
In the citing paper
“Due to the very long telomeres of Mus musculus, critical reduction in telomere length and chromosomal instability is only seen following extensive passage of mTR−/− cells (Niida et al. 1998”
From p53 Deficiency Rescues the Adverse Effects of Telomere Loss and Cooperates with Telomere Dysfunction to Accelerate Carcinogenesis (1999) · cites this paper as Lee et al. 1998
In the citing paper
“This induction of p53 coincides with the dramatic increase in apoptosis (as assessed by TUNEL) and decreased cellularity in the G6 mTR−/− testis (Lee et al. 1998”
From p53 Deficiency Rescues the Adverse Effects of Telomere Loss and Cooperates with Telomere Dysfunction to Accelerate Carcinogenesis (1999) · cites this paper as Lee et al. 1998
In the citing paper
“Loss of telomere function in late-generation (G4 onward) mTR−/− mice has been shown to adversely affect the morphology and physiology of diverse cell types and organ systems (Lee et al. 1998; Rudolph et al. 1999”
From p53 Deficiency Rescues the Adverse Effects of Telomere Loss and Cooperates with Telomere Dysfunction to Accelerate Carcinogenesis (1999) · cites this paper as Lee et al. 1998
In the citing paper
“In the G6 mTR−/− p53+/− intercrosses, we observed an unusually high rate of productive mating pairs (11 of 22 mating pairs) compared to G6 mTR−/− p53+/+ matings (Lee et al. 1998”
From p53 Deficiency Rescues the Adverse Effects of Telomere Loss and Cooperates with Telomere Dysfunction to Accelerate Carcinogenesis (1999) · cites this paper as Lee et al. 1998
In the citing paper
“In mTR−/− mice, a decrease in testis size that correlated with germ cell depletion by histology was first evident in G5 mTR−/− animals and became more prevalent in G6 mTR−/− mice (Lee et al. 1998”
From p53 Deficiency Rescues the Adverse Effects of Telomere Loss and Cooperates with Telomere Dysfunction to Accelerate Carcinogenesis (1999) · cites this paper as Lee et al. 1998
In the citing paper
“In agreement with these findings, studies of telomerase knockout mice revealed short dysfunctional telomeres that profoundly impaired progenitor cell function in actively renewing tissues leading to atrophy and reduced regenerative potential, whereas more quiescent low-turnover tissues such as muscle were unaffected (Allsopp et al., 2003; Lee et al., 1998; Rudolph et al., 1999).”
From Short Telomeres and Stem Cell Exhaustion Model Duchenne Muscular Dystrophy in mdx/mTR Mice (2010) · cites this paper as Lee et al., 1998
In the citing paper
“Of note, late-generation Terc-deficient mice show some signs of accelerated aging (Lee et al., 1998; Rudolph et al., 1999”
From DNA Repair, Genome Stability, and Aging (2005) · cites this paper as Lee et al., 1998
In the citing paper
“Surprisingly, each telomerase component was found to be dispensable for life and these telomerase-knockout mice were remarkably normal (60).”
From Telomeres and telomerase in cancer (2010) · cites this paper as [60]
In the citing paper
“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 [60]
In the citing paper
“The consequent signalling cascades activate checkpoints that induce either cellular senescence or apoptosis, and in at least some contexts both processes occur simultaneously82,85,91,95.”
From The telomere syndromes (2012) · cites this paper as [85]
In the citing paper
“The telomerase-knockout mouse has provided an important model for understanding telomere-mediated disease mechanisms because there is a remarkable convergence with human disease phenotypes (an overview is shown in Table 2)36,82,84,85,97,99–111.”
From The telomere syndromes (2012) · cites this paper as [85]
In the citing paper
“Although it was initially clear that high-turnover tissues are particularly sensitive to telomere length85,101,112”
From The telomere syndromes (2012) · cites this paper as [85]
In the citing paper
“In addition to promoting cell cycle arrest, dysfunctional telomeres can also activate p53-dependent apoptosis, since mice bearing dysfunctional telomeres show increased apoptosis in proliferative cells31-33.”
From Telomere dysfunction and tumour suppression: the senescence connection (2008) · cites this paper as [31]
In the citing paper
“By the sixth generation (G6), increased apoptosis and compromised function were observed in highly proliferative tissues including skin, hematopoietic and reproductive systems31, 42-44.”
From Telomere dysfunction and tumour suppression: the senescence connection (2008) · cites this paper as [31]
In the citing paper
“and the mice were no longer able to reproduce (15).”
From Inhibition of human telomerase in immortal human cells leads to progressive telomere shortening and cell death (1999) · cites this paper as [15]
In the citing paper
“by the seventh generation, highly proliferative organ systems like the testis, bone marrow, and spleen appeared abnormal”
From Inhibition of human telomerase in immortal human cells leads to progressive telomere shortening and cell death (1999) · cites this paper as [15]
In the citing paper
“In particular, mice carrying a homozygous germline deletion of the telomerase RNA component gene (Terc−/−) exhibit critically short telomeres and a premature development of age-related pathologies from the second or third generation [8, 18–20, 51, 70, 72, 101, 103]”
From Senescence-related impairment of autophagy induces toxic intraneuronal amyloid-β accumulation in a mouse model of amyloid pathology (2023) · cites this paper as [70]
In the citing paper
“telomerase-deficient mice with short telomeres show reduced function of various stem cell compartments including those in the bone marrow and skin 58, 60”
From The common biology of cancer and ageing (2007) · cites this paper as [58]
In the citing paper
“the generation and characterization of the telomerase knockout mouse model has been instrumental in demonstrating that short telomeres result in multiple organismal defects caused by defective tissue regeneration 57, 58, 59”
From The common biology of cancer and ageing (2007) · cites this paper as [58]
In the citing paper
“In stem cell and progenitor cell compartments3–5, TERT serves an important role in keeping telomeres sufficiently long and stable to prevent the adverse consequences of dysfunctional telomeres on cell viability and chromosomal stability6–8.”
From Conditional telomerase induction causes proliferation of hair follicle stem cells (2005) · cites this paper as [7]
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“Further evidence for a role of telomerase and telomere length in organ homeostasis comes from the study of telomerase-deficient mice (Terc / mice), which show premature aging and a decreased proliferative potential of adult stem cell populations (Blasco et al., 1997; Lee et al., 1998; Herrera et al., 1999; Samper et a…”
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Shay, J. W., & Roninson, I. B. (2004) · Oncogene · doi:10.1038/sj.onc.1207518 · Cited by 502
“Late-generation telomerase-deficient mice show severe proliferative defects leading to immune dysfunction and failure to reproduce (Blasco et al., 1997; Lee et al., 1998; Chin et al., 1999; Rudolph et al., 1999).”
BackgroundGomes, N. M. V., Ryder, O. A., Houck, M. L., Charter, S. J., Walker, W., Forsyth, N. R., Austad, S. N., Venditti, C., Pagel, M., Shay, J. W., et al. (2011) · Aging Cell · doi:10.1111/j.1474-9726.2011.00718.x · Cited by 464
“This shortening is prevented in the germline and certain stem cells (Lee et al., 1998) by the presence of telomerase.”
BackgroundTelomere Position Effect in Human Cells
Baur, J. A., Zou, Y. S., Shay, J. W., & Wright, W. E. (2001) · Science · doi:10.1126/science.1062329 · Cited by 502
Telomeres, stem cells, senescence, and cancer
Sharpless, N. E., & DePinho, R. A. (2004) · Journal of Clinical Investigation · doi:10.1172/jci20761 · Cited by 488
Self-citationDisease states associated with telomerase deficiency appear earlier in mice with short telomeres
Herrera, E., Samper, E., Martín‐Caballero, J., Flores, J. M., Lee, H., & Blasco, M. A. (1999) · The EMBO Journal · doi:10.1093/emboj/18.11.2950 · Cited by 471
“mTR–/– mice are viable; however, as telomeres shorten and chromosome fusions accumulate with increasing generations, the mTR–/– mice show defects in the reproductive and the hematopoietic system (Blasco et al., 1997; Lee et al., 1998; Rudolph et al., 1999).”
BackgroundInfluentialSelf-citationReplication and protection of telomeres
Verdun, R. E., & Karlseder, J. (2007) · Nature · doi:10.1038/nature05976 · Cited by 463
Effects of Telomerase and Telomere Length on Epidermal Stem Cell Behavior
Flores, I., Cayuela, M. L., & Blasco, M. A. (2005) · Science · doi:10.1126/science.1115025 · Cited by 448
Self-citationTakakura, M., Kyo, S., Kanaya, T., Hirano, H., Takeda, J., Yutsudo, M., & Inoue, M. (1999) · PubMed · Cited by 599
The telomerase reverse transcriptase: components and regulationPreprint
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“This approach has in fact revealed that cells that normally display high proliferation rates in the wild-type mouse are now at a disadvantage in the late backcrosses (Lee et al. 1998).”
BackgroundInhibition of Experimental Liver Cirrhosis in Mice by Telomerase Gene Delivery
Rudolph, K. L., Chang, S., Millard, M., Schreiber-Agus, N., & DePinho, R. A. (2000) · Science · doi:10.1126/science.287.5456.1253 · Cited by 424
Self-citationDyskeratosis Congenita and Cancer in Mice Deficient in Ribosomal RNA Modification
Ruggero, D., Grisendi, S., Piazza, F., Rego, E. M., Mari, F., Rao, P. H., Cordon‐Cardo, C., & Pandolfi, P. P. (2003) · Science · doi:10.1126/science.1079447 · Cited by 450
Choudhury, A. R., Ju, Z., Djojosubroto, M. W., Schienke, A., Lechel, A., Schaetzlein, S., Jiang, H., Stepczynska, A., Wang, C., Buer, J., et al. (2007) · Nature Genetics · doi:10.1038/ng1937 · Cited by 426
“DNA damage signaling in response to telomere dysfunction induces cell cycle arrest, senescence or apoptosi”
BackgroundSelf-citationMultiple Tumor Suppressor Pathways Negatively Regulate Telomerase
Lin, S., & Elledge, S. J. (2003) · Cell · doi:10.1016/s0092-8674(03)00430-6 · Cited by 432
Conditional telomerase induction causes proliferation of hair follicle stem cells
Sarin, K. Y., Cheung, P., Gilison, D., Lee, E., Tennen, R. I., Wang, E., Artandi, M. K., Oro, A. E., & Artandi, S. E. (2005) · Nature · doi:10.1038/nature03836 · Cited by 425
Telomeres and cell senescence—size matters not
Victorelli, S., & Passos, J. F. (2017) · EBioMedicine · doi:10.1016/j.ebiom.2017.03.027 · Cited by 413
“Telomerase knock-out (mTERC−/−) mice which carry a homozygous deletion of the RNA component of telomerase (Blasco et al., 1997) show a generation-dependent telomere shortening, which results in critically short telomeres and both senescence and apoptosis (Lee et al., 1998).”
BackgroundTelomere dysfunction and tumour suppression: the senescence connection
Deng, Y., Chan, S. S., & Chang, S. (2008) · Nature Reviews Cancer · doi:10.1038/nrc2393 · Cited by 411
“In addition to promoting cell cycle arrest, dysfunctional telomeres can also activate p53-dependent apoptosis, as mice bearing dysfunctional telomeres show increased apoptosis in proliferative cell”
BackgroundMechanisms and Regulation of Cellular Senescence
Roger, L., Tomas, F., & Gire, V. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms222313173 · Cited by 395
“Transgenic mouse models without or with inducible telomerase [300,301] allowed establishing a link between short telomeres and the onset of aging phenotypes [300,302,303], progeroid syndromes [304], and chronic inflammatory and degenerative conditions [305,306].”
BackgroundCellular senescence, cancer and aging: the telomere connection
Campisi, J., Kim, S.-H., Lim, C.-S., & Rubio, M. (2001) · Experimental Gerontology · doi:10.1016/s0531-5565(01)00160-7 · Cited by 400
DNA damage checkpoints in stem cells, ageing and cancer
Sperka, T., Wang, J., & Rudolph, K. L. (2012) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3420 · Cited by 393
Axis of ageing: telomeres, p53 and mitochondria
Sahin, E., & DePinho, R. A. (2012) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3352 · Cited by 345
Self-citationTelomerase-Mediated Telomere Addition In Vivo Requires DNA Primase and DNA Polymerases α and δ
Diede, S. J., & Gottschling, D. E. (1999) · Cell · doi:10.1016/s0092-8674(00)81670-0 · Cited by 379
González‐Suárez, E., Samper, E., Ramírez, A., Flores, J. M., Martín‐Caballero, J., Jorcano, J. L., & Blasco, M. A. (2001) · The EMBO Journal · doi:10.1093/emboj/20.11.2619 · Cited by 372
“1997; Lee et al., 1998 ), the absence of telomerase activity has a dramatic inhibitory impact on skin tumorigenesis (Gonza ´lez-Sua ´rez et al., 2000), indicating that tumor formation in skin requires telomere maintenance above a threshold length.”
BackgroundSelf-citationTelomere dysfunction and Atm deficiency compromises organ homeostasis and accelerates ageing
Wong, K.-K., Maser, R. S., Bachoo, R. M., Menon, J., Carrasco, D. R., Gu, Y., Alt, F. W., & DePinho, R. A. (2003) · Nature · doi:10.1038/nature01385 · Cited by 375
“We examined the impact of Atm deficiency as a function of progressive telomere attrition at both the cellular and whole-organism level in mice doubly null for Atm and the telomerase RNA component ( Terc”
BackgroundSelf-citationShort Dysfunctional Telomeres Impair Tumorigenesis in the INK4aΔ2/3 Cancer-Prone Mouse
Greenberg, R. A., Chin, L., Femino, A., Lee, K.-H., Gottlieb, G. J., Singer, R. H., Greider, C. W., & DePinho, R. A. (1999) · Cell · doi:10.1016/s0092-8674(00)80761-8 · Cited by 367
Self-citationEffects of cationic porphyrins as G-quadruplex interactive agents in human tumor cells.
Izbicka, E., Wheelhouse, R. T., Raymond, É., Davidson, K. K., Lawrence, R. A., Sun, D., Windle, B. E., Hurley, L. H., & Hoff, D. D. V. (1999) · PubMed · Cited by 358
Natural and pharmacological regulation of telomerase
Mergny, J. (2002) · Nucleic Acids Research · doi:10.1093/nar/30.4.839 · Cited by 355
Telomerase-deficient mice with short telomeres are resistant to skin tumorigenesis
González-Suárez, E., Samper, E., Flores, J. M., & Blasco, M. A. (2000) · Nature Genetics · doi:10.1038/79089 · Cited by 347
Self-citationTelomeres and age-related disease: how telomere biology informs clinical paradigms
Armanios, M. Y. (2013) · Journal of Clinical Investigation · doi:10.1172/jci66370 · Cited by 351
“Cell type–dependent factors determine whether apoptosis, senescence, or a combined phenotype predominates in response to dysfunctional telomeres (14, 24, 25), although the molecular effectors that discriminate between these pathways are not entirely understood.”
Regulation of human telomerase in homeostasis and disease
Roake, C. M., & Artandi, S. E. (2020) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-020-0234-z · Cited by 356
A Differentiation Checkpoint Limits Hematopoietic Stem Cell Self-Renewal in Response to DNA Damage
Wang, J., Sun, Q., Morita, Y., Jiang, H., Groß, A., Lechel, A., Hildner, K., Guachalla, L. M., Gompf, A., Hartmann, D., et al. (2012) · Cell · doi:10.1016/j.cell.2012.01.040 · Cited by 343
Venteicher, A. S., Meng, Z., Mason, P. J., Veenstra, T. D., & Artandi, S. E. (2008) · Cell · doi:10.1016/j.cell.2008.01.019 · Cited by 329
“These dysfunctional telomeres impair stem cell self-renewal, leading to profound defects in proliferating tissues of telomerase knockout mice (Lee et al., 1998; Allsopp et al., 2003).”
Telomere dysfunction causes alveolar stem cell failure
Alder, J. K., Barkauskas, C. E., Limjunyawong, N., Stanley, S. E., Kembou, F., Tuder, R. M., Hogan, B. L. M., Mitzner, W., & Armanios, M. (2015) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1504780112 · Cited by 339
“In high-turnover epithelial tissues such as the intestinal tract, telomere dysfunction preferentially induces apoptosis (32, 33, 38).”
BackgroundChoi, J., Southworth, L. K., Sarin, K. Y., Venteicher, A. S., Ma, W., Chang, W., Cheung, P., Jun, S., Artandi, M. K., Shah, N., et al. (2008) · PLoS Genetics · doi:10.1371/journal.pgen.0040010 · Cited by 336
“apoptosis and block proliferation [1].”
Telomeres: Cancer to Human Aging
Stewart, S. A., & Weinberg, R. A. (2006) · Annual Review of Cell and Developmental Biology · doi:10.1146/annurev.cellbio.22.010305.104518 · Cited by 349
“…example, studies have demonstrated that mice lacking functional telomerase are unable to maintain proper tissue homeostasis, particularly in tissues of high cell turnover, such as the bone marrow, skin, liver, and gastrointestinal tract (Herrera et al. 1999, Lee et al. 1998, Rudolph et al. 1999).”
BackgroundStress, cell senescence and organismal ageing
de Magalhães, J. P., & Passos, J. F. (2018) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2017.07.001 · Cited by 316
“This in turn results in critically short telomeres which are responsible for an early onset of senescence and apoptosis (Lee et al., 1998) and reduced regenerative capacity of proliferative”
When stem cells grow old: phenotypes and mechanisms of stem cell aging
Schultz, M. B., & Sinclair, D. A. (2016) · Development · doi:10.1242/dev.130633 · Cited by 341
“Only in the sixth generation is stem cell attrition observed, although a skewed HSC lineage potential phenotype can be observed as early as the fourth generation (Ju et al., 2007; Lee et al., 1998).”
BackgroundAllsopp, R. C., Morin, G. B., DePinho, R., Harley, C. B., & Weissman, I. L. (2003) · Blood · doi:10.1182/blood-2002-07-2334 · Cited by 324
Self-citationMechanisms that Regulate Stem Cell Aging and Life Span
Signer, R. A. J., & Morrison, S. J. (2013) · Cell Stem Cell · doi:10.1016/j.stem.2013.01.001 · Cited by 320
“…mice exhibit defects in stem cell function in the forebrain, epidermis, intestinal epithelium, and hematopoietic system through cell-autonomous (Lee et al., 1998; Allsopp et al., 2003; Choudhury et al., 2007; Ferrón et al., 2009; Jaskelioff et al., 2011) and non-cell-autonomous effects on…”
Syndromes of Telomere Shortening
Armanios, M. (2009) · Annual Review of Genomics and Human Genetics · doi:10.1146/annurev-genom-082908-150046 · Cited by 317
“Because of the end-replication problem (24,52), telomeres shorten successively with each cell division, and short telomeres activate a p53-dependent checkpoint that leads to apoptosis or senescence (Figure 1) (7,11,20,31,34,40,69).”
BackgroundConstitutive telomerase expression promotes mammary carcinomas in aging mice
Artandi, S. E., Alson, S., Tietze, M. K., Sharpless, N. E., Ye, S., Greenberg, R. A., Castrillon, D. H., Horner, J. W., Weiler, S. R., Carrasco, R. D., et al. (2002) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.112515399 · Cited by 317
Self-citationTelomere Length Dynamics and Chromosomal Instability in Cells Derived from Telomerase Null Mice
Hande, M. P., Samper, E., Lansdorp, P., & Blasco, M. A. (1999) · The Journal of Cell Biology · doi:10.1083/jcb.144.4.589 · Cited by 313
“Such variation between littermates could be the basis for the fact that only a percentage of KO-G6 mice show defects associated with telomere loss (Lee et al., 1998; Herrera el al., 1999).”
InfluentialSelf-citationShort Telomeres Limit Tumor Progression In Vivo by Inducing Senescence
Feldser, D. M., & Greider, C. W. (2007) · Cancer Cell · doi:10.1016/j.ccr.2007.02.026 · Cited by 314
Self-citationInvolvement of 14‐3‐3 proteins in nuclear localization of telomerase
Seimiya, H., Sawada, H., Muramatsu, Y., Shimizu, M., Ohko, K., Yamane, K., & Tsuruo, T. (2000) · The EMBO Journal · doi:10.1093/emboj/19.11.2652 · Cited by 318
Leri, A., Franco, S., Zacheo, A., Barlucchi, L., Chimenti, S., Limana, F., Nadal‐Ginard, B., Kajstura, J., Anversa, P., & Blasco, M. A. (2003) · The EMBO Journal · doi:10.1093/emboj/cdg013 · Cited by 313
Self-citationHodes, R. J., Hathcock, K. S., & Weng, N. (2002) · Nature reviews. Immunology · doi:10.1038/nri890 · Cited by 317
“However, the breeding of successive generations of telomerase-deficient mice results in the progressive shortening of telomeres and, eventually (after ∼5–6 generations), both males and females are sterile, apparently owing to replicative failure and the increased apoptosis of germ-line cell”
BackgroundShort Telomeres, even in the Presence of Telomerase, Limit Tissue Renewal Capacity
Hao, L.-Y., Armanios, M., Strong, M. A., Karim, B., Feldser, D. M., Huso, D., & Greider, C. W. (2005) · Cell · doi:10.1016/j.cell.2005.11.020 · Cited by 302
“In mice, the apoptosis leads to loss of germ cells and consequently decreased fertility with each generation (Lee et al., 1998; Hemann et al., 2001b).”
BackgroundSelf-citationTelomere dysfunction impairs DNA repair and enhances sensitivity to ionizing radiation
Wong, K.-K., Chang, S., Weiler, S. R., Ganesan, S., Chaudhuri, J., Zhu, C., Artandi, S. E., Rudolph, K. L., Gottlieb, G. J., Chin, L., et al. (2000) · Nature Genetics · doi:10.1038/79232 · Cited by 309
“We used the telomerase-deficient mouse, in which telomeres are eroded to a critically short length through serial Terc −/− intercrosses to produce successive generations (G1 Terc −/− through G6 Terc −/− ) of Terc −/− mic”
MethodSelf-citation
Metadata
- Authors
- Lee, H.-W., Blasco, M. A., Gottlieb, G. J., Horner, J. W., Greider, C. W., & DePinho, R. A.
- Affiliations
- Albert Einstein College of Medicine (US)
- Quest Diagnostics (United States) (US)
- Johns Hopkins University (US)
- Venue
- Nature
- Published
- 1998-04
- Volume
- 392
- Issue
- 6676
- Pages
- 569-574
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W1612842202
- Cited by
- 1,270
- References
- 40
- Citations by year
- 2026: 12 · 2025: 16 · 2024: 23 · 2023: 24 · 2022: 25 · 2021: 40 · 2020: 25 · 2019: 30 · 2018: 38 · 2017: 26 · 2016: 40 · 2015: 45 · 2014: 31 · 2013: 42 · 2012: 49
- FWCI
- 45.54
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- 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
- telomerase, telomeres, spermatogenesis, apoptosis, cell proliferation, testis, hematopoietic cells, bone marrow, spleen, chromosome fusion, chromosome loss, genome stability, tissue renewal, mice
- MeSH terms
- Animals, Cell Division, Chromosome Banding, Female, Embryonic and Fetal Development, Hematopoiesis, Hematopoietic Stem Cells, Lymphocytes, Male, Mice, Inbred C57BL, Ovary, Testis, Telomere, Apoptosis, Telomerase, Mice
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