<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Yu VW</submitter><funding>Tosteson &amp;amp; Fund for Medical Discovery Fellowship</funding><funding>Proton Therapy Research and Treatment Center</funding><funding>NHLBI</funding><funding>MGH Federal Share</funding><funding>NHLBI NIH HHS</funding><funding>BD Biosciences</funding><funding>Bullock-Wellman Fellowship Award</funding><funding>NCI NIH HHS</funding><pagination>318-9</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4583650</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>5</volume><pubmed_abstract>The bone marrow niche is recognized as a central player in maintaining and regulating the behavior of hematopoietic stem and progenitor cells. Specific gain-of and loss-of function experiments perturbing a range of osteolineage cells or their secreted proteins had been shown to affect stem cell maintenance (Calvi et al, 2003 [1]; Stier et al., 2005 [2]; Zhang et al., 2003 [3]; Nilsson et al., 2005 [4]; Greenbaum et al., 2013 [5]) and engraftment (Adam et al., 2006, 2009 [6,7]). We used specific in vivo cell deletion approaches to dissect the niche cell-parenchymal cell dependency in a complex bone marrow microenvironment. Endogenous deletion of osteocalcin-expressing (Ocn(+)) cells led to a loss of T immune cells (Yu et al., 2015 [8]. Ocn(+) cells express the Notch ligand DLL4 to communica</pubmed_abstract><journal>Genomics data</journal><pubmed_title>Transcriptome comparison of distinct osteolineage subsets in the hematopoietic stem cell niche using a triple fluorescent transgenic mouse model.</pubmed_title><pmcid>PMC4583650</pmcid><funding_grant_id>U01 HL100402</funding_grant_id><funding_grant_id>R01 HL044851</funding_grant_id><funding_grant_id>HL044851</funding_grant_id><funding_grant_id>C06 CA059267</funding_grant_id><funding_grant_id>HL097794</funding_grant_id><funding_grant_id>R01 HL097794</funding_grant_id><funding_grant_id>HL100402</funding_grant_id><pubmed_authors>Lymperi S</pubmed_authors><pubmed_authors>Scadden DT</pubmed_authors><pubmed_authors>Ferraro F</pubmed_authors><pubmed_authors>Yu VW</pubmed_authors></additional><is_claimable>false</is_claimable><name>Transcriptome comparison of distinct osteolineage subsets in the hematopoietic stem cell niche using a triple fluorescent transgenic mouse model.</name><description>The bone marrow niche is recognized as a central player in maintaining and regulating the behavior of hematopoietic stem and progenitor cells. Specific gain-of and loss-of function experiments perturbing a range of osteolineage cells or their secreted proteins had been shown to affect stem cell maintenance (Calvi et al, 2003 [1]; Stier et al., 2005 [2]; Zhang et al., 2003 [3]; Nilsson et al., 2005 [4]; Greenbaum et al., 2013 [5]) and engraftment (Adam et al., 2006, 2009 [6,7]). We used specific in vivo cell deletion approaches to dissect the niche cell-parenchymal cell dependency in a complex bone marrow microenvironment. Endogenous deletion of osteocalcin-expressing (Ocn(+)) cells led to a loss of T immune cells (Yu et al., 2015 [8]. Ocn(+) cells express the Notch ligand DLL4 to communica</description><dates><release>2015-01-01T00:00:00Z</release><publication>2015 Sep</publication><modification>2025-04-22T14:18:14.966Z</modification><creation>2019-06-06T14:54:40Z</creation></dates><accession>S-EPMC4583650</accession><cross_references><pubmed>26484277</pubmed><doi>10.1016/j.gdata.2015.06.001</doi></cross_references></HashMap>