title: GATA-2 mediated regulation of normal hematopoietic stem/progenitor cell function, myelodysplasia and myeloid leukemia.
abstract: Unremitting blood cell production throughout the lifetime of an organism is reliant on hematopoietic stem cells (HSCs). A rare and relatively quiescent cell type, HSCs are, on entry into cell cycle fated to self-renew, undergo apoptosis or differentiate to progenitors (HPCs) that eventually yield specific classes of blood cells. Disruption of these HSC fate decisions is considered to be fundamental to the development of leukemia. Much effort has therefore been placed on understanding the molecular pathways that regulate HSC fate decisions and how these processes are undermined in leukemia. Transcription factors have emerged as critical regulators in this respect. Here we review the participation of zinc finger transcription factor GATA-2 in regulating normal hematopoietic stem and progenitor cell functionality, myelodysplasia and myeloid leukemia.
authors.affiliation: National Institutes of Health Center for Biomedical Research Excellence in Stem Cell Biology, Roger Williams Medical Center, Boston University School of Medicine, Providence, RI 02908, United States. neilr@bu.edu
authors.forename: Neil P
authors.initials: NP
authors.lastname: Rodrigues
authors.forename: Alex J
authors.initials: AJ
authors.lastname: Tipping
authors.forename: Zhengke
authors.initials: Z
authors.lastname: Wang
authors.forename: Tariq
authors.initials: T
authors.lastname: Enver
mesh_terms: D000818:Animals; D002454:Cell Differentiation / Q000235:genetics; D002470:Cell Survival / Q000235:genetics; D002471:Cell Transformation, Neoplastic / Q000235:genetics; D050989:GATA2 Transcription Factor / Q000235:genetics / Q000378:metabolism*; D006412:Hematopoietic Stem Cells / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D007951:Leukemia, Myeloid / Q000473:pathology*; D009154:Mutation / Q000235:genetics; D009190:Myelodysplastic Syndromes / Q000473:pathology*
chemical_list: D050989:GATA2 Transcription Factor