GATA-2 mediated regulation of normal hematopoietic stem/progenitor cell function, myelodysplasia and myeloid leukemia
Identifieur interne : 004929 ( Ncbi/Checkpoint ); précédent : 004928; suivant : 004930GATA-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 :
- The international journal of biochemistry & cell biology [ 1357-2725 ] ; 2011.
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
Affiliations:
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<front><div type="abstract" xml:lang="en"><p id="P2">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.</p>
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