<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Geiger H</submitter><funding>NIA NIH HHS</funding><pagination>5102-7</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC555968</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>102(14)</volume><pubmed_abstract>Until recently, stem cells were thought to be endowed with unlimited self-renewal capacity and, thus, assumed exempt from aging. But accumulating evidence over the past decade compellingly argues that a measurable and progressive replicative impairment in the hematopoietic, intestinal, and muscle stem cell activity exists from adulthood to old age, resulting in a decline in stem cell function and rendering stem cell aging as the possible link between cellular aging and organismal aging. By using a previously uncharacterized congenic animal model to study genetic regulation of hematopoietic stem cell aging, we have demonstrated definitively that a locus on murine chromosome 2 regulates hematopoietic stem cell aging. In addition to demonstrating that hematopoietic stem cell aging is regulate</pubmed_abstract><journal>Proceedings of the National Academy of Sciences of the United States of America</journal><pubmed_title>Regulation of hematopoietic stem cell aging in vivo by a distinct genetic element.</pubmed_title><pmcid>PMC555968</pmcid><funding_grant_id>AG16653</funding_grant_id><funding_grant_id>R01 AG020917</funding_grant_id><funding_grant_id>AG20917</funding_grant_id><pubmed_authors>Van Zant G</pubmed_authors><pubmed_authors>Geiger H</pubmed_authors><pubmed_authors>Rennebeck G</pubmed_authors></additional><is_claimable>false</is_claimable><name>Regulation of hematopoietic stem cell aging in vivo by a distinct genetic element.</name><description>Until recently, stem cells were thought to be endowed with unlimited self-renewal capacity and, thus, assumed exempt from aging. But accumulating evidence over the past decade compellingly argues that a measurable and progressive replicative impairment in the hematopoietic, intestinal, and muscle stem cell activity exists from adulthood to old age, resulting in a decline in stem cell function and rendering stem cell aging as the possible link between cellular aging and organismal aging. By using a previously uncharacterized congenic animal model to study genetic regulation of hematopoietic stem cell aging, we have demonstrated definitively that a locus on murine chromosome 2 regulates hematopoietic stem cell aging. In addition to demonstrating that hematopoietic stem cell aging is regulate</description><dates><release>2005-01-01T00:00:00Z</release><publication>2005 Apr</publication><modification>2025-06-01T00:32:18.344Z</modification><creation>2025-06-01T00:32:18.344Z</creation></dates><accession>S-EPMC555968</accession><cross_references><pubmed>15788535</pubmed><doi>10.1073/pnas.0408654102</doi></cross_references></HashMap>