<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Liu F</submitter><funding>NCATS NIH HHS</funding><funding>NHLBI NIH HHS</funding><funding>NCI NIH HHS</funding><funding>NIAMS NIH HHS</funding><pagination>3295-305</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3321855</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>119(14)</volume><pubmed_abstract>Two distinct types of Flk-1(+) mesoderm, hemangiogenic and cardiogenic, are thought to contribute to blood, vessel, and cardiac cell lineages. However, our understanding of how Flk-1(+) mesoderm is specified is currently limited. In the present study, we investigated whether ER71, an Ets transcription factor essential for hematopoietic and endothelial cell lineage development, could modulate the hemangiogenic or cardiogenic outcome of the Flk-1(+) mesoderm. We show that Flk-1(+) mesoderm can be divided into Flk-1(+)PDGFRα(-) hemangiogenic and Flk-1(+)PDGFRα(+) cardiogenic mesoderm. ER71-deficient embryonic stem cells produced only the Flk-1(+)PDGFRα(+) cardiogenic mesoderm, which generated SMCs and cardiomyocytes. Enforced ER71 expression in the wild-type embryonic stem cells skewed toward</pubmed_abstract><journal>Blood</journal><pubmed_title>ER71 specifies Flk-1+ hemangiogenic mesoderm by inhibiting cardiac mesoderm and Wnt signaling.</pubmed_title><pmcid>PMC3321855</pmcid><funding_grant_id>R01 HL063736</funding_grant_id><funding_grant_id>HL034161</funding_grant_id><funding_grant_id>P30 CA091842</funding_grant_id><funding_grant_id>P30 AR048335</funding_grant_id><funding_grant_id>R29 HL055337</funding_grant_id><funding_grant_id>R01 HL055337</funding_grant_id><funding_grant_id>HL55337</funding_grant_id><funding_grant_id>HL63736</funding_grant_id><funding_grant_id>P30-CA91842</funding_grant_id><funding_grant_id>P30-AR48335</funding_grant_id><funding_grant_id>UL1 TR000448</funding_grant_id><funding_grant_id>R01 HL034161</funding_grant_id><pubmed_authors>Vittet D</pubmed_authors><pubmed_authors>Lim DS</pubmed_authors><pubmed_authors>Choi K</pubmed_authors><pubmed_authors>Wang W</pubmed_authors><pubmed_authors>Chang LW</pubmed_authors><pubmed_authors>Kang I</pubmed_authors><pubmed_authors>Park C</pubmed_authors><pubmed_authors>Liu F</pubmed_authors><pubmed_authors>Lee D</pubmed_authors><pubmed_authors>Nerbonne JM</pubmed_authors></additional><is_claimable>false</is_claimable><name>ER71 specifies Flk-1+ hemangiogenic mesoderm by inhibiting cardiac mesoderm and Wnt signaling.</name><description>Two distinct types of Flk-1(+) mesoderm, hemangiogenic and cardiogenic, are thought to contribute to blood, vessel, and cardiac cell lineages. However, our understanding of how Flk-1(+) mesoderm is specified is currently limited. In the present study, we investigated whether ER71, an Ets transcription factor essential for hematopoietic and endothelial cell lineage development, could modulate the hemangiogenic or cardiogenic outcome of the Flk-1(+) mesoderm. We show that Flk-1(+) mesoderm can be divided into Flk-1(+)PDGFRα(-) hemangiogenic and Flk-1(+)PDGFRα(+) cardiogenic mesoderm. ER71-deficient embryonic stem cells produced only the Flk-1(+)PDGFRα(+) cardiogenic mesoderm, which generated SMCs and cardiomyocytes. Enforced ER71 expression in the wild-type embryonic stem cells skewed toward</description><dates><release>2012-01-01T00:00:00Z</release><publication>2012 Apr</publication><modification>2026-04-29T15:41:27.019Z</modification><creation>2026-04-07T15:24:44.587Z</creation></dates><accession>S-EPMC3321855</accession><cross_references><pubmed>22343916</pubmed><doi>10.1182/blood-2012-01-403766</doi></cross_references></HashMap>