<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Suh HC</submitter><funding>NCI NIH HHS</funding><pagination>1186-95</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2723014</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>114(6)</volume><pubmed_abstract>Development of hematopoietic stem cells (HSCs) and their immediate progeny is maintained by the interaction with cells in the microenvironment. We found that hematopoiesis was dysregulated in Id1(-/-) mice. Although the frequency of HSCs in Id1(-/-) bone marrow was increased, their total numbers remained unchanged as the result of decreased bone marrow cellularity. In addition, the ability of Id1(-/-) HSCs to self-renew was normal, suggesting Id1 does not affect HSC function. Id1(-/-) progenitors showed increased cycling in vivo but not in vitro, suggesting cell nonautonomous mechanisms for the increased cycling. Id1(-/-) HSCs developed normally when transplanted into Id1(+/+) mice, whereas the development of Id1(+/+) HSCs was impaired in Id1(-/-) recipients undergoing transplantation and </pubmed_abstract><journal>Blood</journal><pubmed_title>Cell-nonautonomous function of Id1 in the hematopoietic progenitor cell niche.</pubmed_title><pmcid>PMC2723014</pmcid><funding_grant_id>N01-CO-12 400</funding_grant_id><pubmed_authors>Gooya J</pubmed_authors><pubmed_authors>Keller JR</pubmed_authors><pubmed_authors>Suh HC</pubmed_authors><pubmed_authors>Lee M</pubmed_authors><pubmed_authors>Klarmann KD</pubmed_authors><pubmed_authors>Ji M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Cell-nonautonomous function of Id1 in the hematopoietic progenitor cell niche.</name><description>Development of hematopoietic stem cells (HSCs) and their immediate progeny is maintained by the interaction with cells in the microenvironment. We found that hematopoiesis was dysregulated in Id1(-/-) mice. Although the frequency of HSCs in Id1(-/-) bone marrow was increased, their total numbers remained unchanged as the result of decreased bone marrow cellularity. In addition, the ability of Id1(-/-) HSCs to self-renew was normal, suggesting Id1 does not affect HSC function. Id1(-/-) progenitors showed increased cycling in vivo but not in vitro, suggesting cell nonautonomous mechanisms for the increased cycling. Id1(-/-) HSCs developed normally when transplanted into Id1(+/+) mice, whereas the development of Id1(+/+) HSCs was impaired in Id1(-/-) recipients undergoing transplantation and </description><dates><release>2009-01-01T00:00:00Z</release><publication>2009 Aug</publication><modification>2025-04-05T15:10:46.913Z</modification><creation>2019-03-27T00:24:06Z</creation></dates><accession>S-EPMC2723014</accession><cross_references><pubmed>19478045</pubmed><doi>10.1182/blood-2008-09-179788</doi></cross_references></HashMap>