{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Eaton N"],"funding":["National Heart, Lung, and Blood Institute","NHLBI NIH HHS","American Society of Hematology"],"pagination":["959806"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9468709"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12"],"pubmed_abstract":["<i>Dnm2<sup>fl/fl</sup> Pf4-Cre</i> (<i>Dnm2<sup>Plt-/-</sup></i> ) mice lacking the endocytic GTPase dynamin 2 (DNM2) in platelets and megakaryocytes (MKs) develop hallmarks of myelofibrosis. At the cellular level, the tyrosine kinase JAK2 is constitutively active but decreased in expression in <i>Dnm2<sup>Plt-/-</sup></i> platelets. Additionally, <i>Dnm2<sup>Plt-/-</sup></i> platelets cannot endocytose the thrombopoietin (TPO) receptor Mpl, leading to elevated circulating TPO levels. Here, we assessed whether the hyperproliferative phenotype of <i>Dnm2<sup>Plt-/-</sup></i> mice was due to JAK2 constitutive activation or to elevated circulating TPO levels. In unstimulated <i>Dnm2<sup>Plt-/-</sup></i> platelets, STAT3 and, to a lower extent, STAT5 were phosphorylated, but their phosphoryla"],"journal":["Frontiers in oncology"],"pubmed_title":["Endocytosis of the thrombopoietin receptor Mpl regulates megakaryocyte and erythroid maturation in mice."],"pmcid":["PMC9468709"],"funding_grant_id":["P01 HL046925","K12 HL141954","P01 HL151333","R01 HL126743","HL046925, HL089224, HL141954, HL151333, HL126743","R01 HL089224"],"pubmed_authors":["Hoffmeister KM","Lee-Sundlov MM","Boyd EK","Falet H","Sola-Visner MC","Zheng S","Biswas R","Ramsey HE","Dlugi TA","Eaton N","Burns RT"],"additional_accession":[]},"is_claimable":false,"name":"Endocytosis of the thrombopoietin receptor Mpl regulates megakaryocyte and erythroid maturation in mice.","description":"<i>Dnm2<sup>fl/fl</sup> Pf4-Cre</i> (<i>Dnm2<sup>Plt-/-</sup></i> ) mice lacking the endocytic GTPase dynamin 2 (DNM2) in platelets and megakaryocytes (MKs) develop hallmarks of myelofibrosis. At the cellular level, the tyrosine kinase JAK2 is constitutively active but decreased in expression in <i>Dnm2<sup>Plt-/-</sup></i> platelets. Additionally, <i>Dnm2<sup>Plt-/-</sup></i> platelets cannot endocytose the thrombopoietin (TPO) receptor Mpl, leading to elevated circulating TPO levels. Here, we assessed whether the hyperproliferative phenotype of <i>Dnm2<sup>Plt-/-</sup></i> mice was due to JAK2 constitutive activation or to elevated circulating TPO levels. In unstimulated <i>Dnm2<sup>Plt-/-</sup></i> platelets, STAT3 and, to a lower extent, STAT5 were phosphorylated, but their phosphoryla","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022","modification":"2026-04-08T11:56:08.074Z","creation":"2025-02-19T03:29:19.768Z"},"accession":"S-EPMC9468709","cross_references":{"pubmed":["36110936"],"doi":["10.3389/fonc.2022.959806"]}}