GATA family transcriptional factors: emerging suspects in hematologic disorders
Identifieur interne : 001D57 ( Main/Exploration ); précédent : 001D56; suivant : 001D58GATA family transcriptional factors: emerging suspects in hematologic disorders
Auteurs : Juehua Gao [États-Unis] ; Yi-Hua Chen [États-Unis] ; Loann C. Peterson [États-Unis]Source :
- Experimental Hematology & Oncology [ 2162-3619 ] ; 2015.
Abstract
GATA transcription factors are zinc finger DNA binding proteins that regulate transcription during development and cell differentiation. The three important GATA transcription factors GATA1, GATA2 and GATA3 play essential roles in the development and maintenance of hematopoietic systems. GATA1 is required for the erythroid and megakaryocytic commitment during hematopoiesis. GATA2 is crucial for the proliferation and survival of early hematopoietic cells, and is also involved in lineage specific transcriptional regulation as the dynamic partner of GATA1. GATA3 plays an essential role in T lymphoid cell development and immune regulation. As a result, mutations in genes encoding the GATA transcription factors or alteration in the protein expression level or their function have been linked to a variety of human hematologic disorders. In this review, we summarized the current knowledge regarding the disrupted biologic function of GATA in various hematologic disorders.
Url:
DOI: 10.1186/s40164-015-0024-z
PubMed: 26445707
PubMed Central: 4594744
Affiliations:
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Huron Street, Chicago, IL 60611 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Illinois</region></placeName><wicri:cityArea>Department of Pathology, Northwestern University Feinberg School of Medicine, 251 E. Huron Street, Chicago</wicri:cityArea></affiliation></author><author><name sortKey="Peterson, Loann C" sort="Peterson, Loann C" uniqKey="Peterson L" first="Loann C." last="Peterson">Loann C. Peterson</name><affiliation wicri:level="2"><nlm:aff id="Aff1">Department of Pathology, Northwestern University Feinberg School of Medicine, 251 E. Huron Street, Chicago, IL 60611 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Illinois</region></placeName><wicri:cityArea>Department of Pathology, Northwestern University Feinberg School of Medicine, 251 E. 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Huron Street, Chicago, IL 60611 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Illinois</region></placeName><wicri:cityArea>Department of Pathology, Northwestern University Feinberg School of Medicine, 251 E. Huron Street, Chicago</wicri:cityArea></affiliation></author><author><name sortKey="Chen, Yi Hua" sort="Chen, Yi Hua" uniqKey="Chen Y" first="Yi-Hua" last="Chen">Yi-Hua Chen</name><affiliation wicri:level="2"><nlm:aff id="Aff1">Department of Pathology, Northwestern University Feinberg School of Medicine, 251 E. Huron Street, Chicago, IL 60611 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Illinois</region></placeName><wicri:cityArea>Department of Pathology, Northwestern University Feinberg School of Medicine, 251 E. Huron Street, Chicago</wicri:cityArea></affiliation></author><author><name sortKey="Peterson, Loann C" sort="Peterson, Loann C" uniqKey="Peterson L" first="Loann C." last="Peterson">Loann C. Peterson</name><affiliation wicri:level="2"><nlm:aff id="Aff1">Department of Pathology, Northwestern University Feinberg School of Medicine, 251 E. Huron Street, Chicago, IL 60611 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Illinois</region></placeName><wicri:cityArea>Department of Pathology, Northwestern University Feinberg School of Medicine, 251 E. Huron Street, Chicago</wicri:cityArea></affiliation></author></analytic><series><title level="j">Experimental Hematology & Oncology</title><idno type="eISSN">2162-3619</idno><imprint><date when="2015">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>GATA transcription factors are zinc finger DNA binding proteins that regulate transcription during development and cell differentiation. The three important GATA transcription factors GATA1, GATA2 and GATA3 play essential roles in the development and maintenance of hematopoietic systems. GATA1 is required for the erythroid and megakaryocytic commitment during hematopoiesis. GATA2 is crucial for the proliferation and survival of early hematopoietic cells, and is also involved in lineage specific transcriptional regulation as the dynamic partner of GATA1. GATA3 plays an essential role in T lymphoid cell development and immune regulation. As a result, mutations in genes encoding the GATA transcription factors or alteration in the protein expression level or their function have been linked to a variety of human hematologic disorders. 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