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GATA-2 mediated regulation of normal hematopoietic stem/progenitor cell function, myelodysplasia and myeloid leukemia

Identifieur interne : 004F10 ( Main/Merge ); précédent : 004F09; suivant : 004F11

GATA-2 mediated regulation of normal hematopoietic stem/progenitor cell function, myelodysplasia and myeloid leukemia

Auteurs : Neil P. Rodrigues [États-Unis] ; Alex J. Tipping [Royaume-Uni] ; Zhengke Wang [États-Unis] ; Tariq Enver [Royaume-Uni]

Source :

RBID : PMC:3319732

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 harbored in adult bone marrow, 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 cell 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 cell fate decisions and how these processes are undermined during 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.


Url:
DOI: 10.1016/j.biocel.2011.12.004
PubMed: 22192845
PubMed Central: 3319732

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PMC:3319732

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