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Prepublished online as a Blood First Edition Paper on March 27, 2003; DOI 10.1182/blood-2002-07-2334. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-07-2334v1 102/2/517    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Allsopp, R. C. Articles by Weissman, I. L. Search for Related Content PubMed PubMed Citation Articles by Allsopp, R. C. Articles by Weissman, I. L. Related Collections Hematopoiesis and Stem Cells Transplantation Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 July 2003, Vol. 102, No. 2, pp. 517-520 HEMATOPOIESIS Brief report Telomerase is required to slow telomere shortening and extend replicative lifespan of HSCs during serial transplantation Richard C. Allsopp, Gregg B. Morin, Ronald DePinho, Calvin B. Harley, and Irving L. Weissman From the Beckman Center, Pathology Department, Stanford University School of Medicine, CA; Geron, Menlo Park, CA; and the Dana-Farber Cancer Institute, Harvard University, Boston, MA. Telomere shortening ultimately limits the replicative life span of cultured human somatic cells. Telomeres also shorten during replicative aging in vivo in hematopoietic cells, including early hematopoietic progenitors and hematopoietic stem cells (HSCs), from humans and mice, despite readily detectable levels of telomerase in these cells. To assess the relevance of telomerase to the long-term replicative capacity of HSCs in vivo, we serially transplanted HSCs from wild-type and telomerase-deficient mice until exhaustion and monitored telomere length in HSCs during this process. Telomerase-deficient HSCs could be serially transplanted for only 2 rounds, whereas wild-type HSCs could be serially transplanted for at least 4 rounds. Furthermore, the rate of telomere shortening was increased approximately 2-fold during serial transplantation of telomerase-deficient HSCs. These findings suggest that one role for telomerase in the HSC is to partially counter the rate of telomere shortening during division of HSCs, thereby preventing premature loss of telomere function and providing added replicative capacity. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D. Hockemeyer, W. Palm, R. C. Wang, S. S. Couto, and T. de Lange Engineered telomere degradation models dyskeratosis congenita Genes & Dev., July 1, 2008; 22(13): 1773 - 1785. [Abstract] [Full Text] [PDF] F. D. Goldman, G. Aubert, A. J. Klingelhutz, M. Hills, S. R. Cooper, W. S. Hamilton, A. J. Schlueter, K. Lambie, C. J. Eaves, and P. M. Lansdorp Characterization of primitive hematopoietic cells from patients with dyskeratosis congenita Blood, May 1, 2008; 111(9): 4523 - 4531. [Abstract] [Full Text] [PDF] G. Aubert and P. M. Lansdorp Telomeres and Aging Physiol Rev, April 1, 2008; 88(2): 557 - 579. 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