GATA-2 mediated regulation of normal hematopoietic stem/progenitor cell function, myelodysplasia and myeloid leukemia
Identifieur interne : 003A36 ( Pmc/Curation ); précédent : 003A35; suivant : 003A37GATA-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
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Rodrigues</name><affiliation wicri:level="1"><nlm:aff id="A1">National Institutes of Health (NIH) Center for Biomedical Research Excellence (COBRE) in Stem Cell Biology, Roger Williams Medical Center, Boston University School of Medicine, Providence, RI 02908, United States of America</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>National Institutes of Health (NIH) Center for Biomedical Research Excellence (COBRE) in Stem Cell Biology, Roger Williams Medical Center, Boston University School of Medicine, Providence, RI 02908</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="A2">Department of Dermatology, Boston University Medical Center, Boston, MA 02118, United States of America</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Dermatology, Boston University Medical Center, Boston, MA 02118</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="A3">Center for Regenerative Medicine, Boston University School of Medicine, Boston, MA 02118, United States of America</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Center for Regenerative Medicine, Boston University School of Medicine, Boston, MA 02118</wicri:regionArea></affiliation></author><author><name sortKey="Tipping, Alex J" sort="Tipping, Alex J" uniqKey="Tipping A" first="Alex J." last="Tipping">Alex J. 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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></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">9508482</journal-id><journal-id journal-id-type="pubmed-jr-id">8630</journal-id><journal-id journal-id-type="nlm-ta">Int J Biochem Cell Biol</journal-id><journal-id journal-id-type="iso-abbrev">Int. J. Biochem. Cell Biol.</journal-id><journal-title-group><journal-title>The international journal of biochemistry & cell biology</journal-title></journal-title-group><issn pub-type="ppub">1357-2725</issn><issn pub-type="epub">1878-5875</issn></journal-meta><article-meta><article-id pub-id-type="pmid">22192845</article-id><article-id pub-id-type="pmc">3319732</article-id><article-id pub-id-type="doi">10.1016/j.biocel.2011.12.004</article-id><article-id pub-id-type="manuscript">NIHMS345307</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>GATA-2 mediated regulation of normal hematopoietic stem/progenitor cell function, myelodysplasia and myeloid leukemia</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Rodrigues</surname><given-names>Neil P.</given-names></name><xref ref-type="aff" rid="A1">1</xref><xref ref-type="aff" rid="A2">2</xref><xref ref-type="aff" rid="A3">3</xref><xref rid="FN1" ref-type="author-notes">*</xref></contrib><contrib contrib-type="author"><name><surname>Tipping</surname><given-names>Alex J.</given-names></name><xref ref-type="aff" rid="A4">4</xref></contrib><contrib contrib-type="author"><name><surname>Wang</surname><given-names>Zhengke</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Enver</surname><given-names>Tariq</given-names></name><xref ref-type="aff" rid="A4">4</xref></contrib></contrib-group><aff id="A1"><label>1</label>National Institutes of Health (NIH) Center for Biomedical Research Excellence (COBRE) in Stem Cell Biology, Roger Williams Medical Center, Boston University School of Medicine, Providence, RI 02908, United States of America</aff><aff id="A2"><label>2</label>Department of Dermatology, Boston University Medical Center, Boston, MA 02118, United States of America</aff><aff id="A3"><label>3</label>Center for Regenerative Medicine, Boston University School of Medicine, Boston, MA 02118, United States of America</aff><aff id="A4"><label>4</label>University College London (UCL) Cancer Institute, London, United Kingdom</aff><author-notes><corresp id="FN1"><label>*</label>Address for correspondence: Neil P. Rodrigues, PhD, NIH COBRE at Roger Williams Medical Center, Boston University School of Medicine, Prior Office 121A, 825 Chalkstone Ave, Providence, RI 02908 USA, Phone: +1 401 456-5367, Fax: +1 401 456-5759, <email>neilr@bu.edu</email></corresp></author-notes><pub-date pub-type="nihms-submitted"><day>30</day><month>12</month><year>2011</year></pub-date><pub-date pub-type="epub"><day>14</day><month>12</month><year>2011</year></pub-date><pub-date pub-type="ppub"><month>3</month><year>2012</year></pub-date><pub-date pub-type="pmc-release"><day>01</day><month>3</month><year>2013</year></pub-date><volume>44</volume><issue>3</issue><fpage>457</fpage><lpage>460</lpage><permissions><copyright-statement>© 2011 Elsevier Ltd. All rights reserved.</copyright-statement><copyright-year>2011</copyright-year></permissions><abstract><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></abstract><kwd-group><kwd>GATA-2</kwd><kwd>hematopoietic stem cells</kwd><kwd>myelodysplasia</kwd><kwd>myeloid leukemia</kwd></kwd-group><funding-group><award-group><funding-source country="United States">National Center for Research Resources : NCRR</funding-source><award-id>P20 RR018757-09 || RR</award-id></award-group></funding-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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