{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Suh HC"],"funding":["NCI NIH HHS"],"pagination":["1186-95"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC2723014"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["114(6)"],"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 "],"journal":["Blood"],"pubmed_title":["Cell-nonautonomous function of Id1 in the hematopoietic progenitor cell niche."],"pmcid":["PMC2723014"],"funding_grant_id":["N01-CO-12 400"],"pubmed_authors":["Gooya J","Keller JR","Suh HC","Lee M","Klarmann KD","Ji M"],"additional_accession":[]},"is_claimable":false,"name":"Cell-nonautonomous function of Id1 in the hematopoietic progenitor cell niche.","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 ","dates":{"release":"2009-01-01T00:00:00Z","publication":"2009 Aug","modification":"2025-04-05T15:10:46.913Z","creation":"2019-03-27T00:24:06Z"},"accession":"S-EPMC2723014","cross_references":{"pubmed":["19478045"],"doi":["10.1182/blood-2008-09-179788"]}}