GATA1 in normal and malignant hematopoiesis

John D. Crispino*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

149 Scopus citations

Abstract

In the late 1980s, several research groups independently discovered the founding member of the GATA family of transcription factors, GATA-1. Each group had evidence that GATA-1 played an important role in erythroid gene expression, but little did they know that it would turn out to be a key regulator of development of not only red blood cells, but of several other hematopoietic cell types as well. Furthermore, few would have guessed that missense mutations in GATA1 would cause inherited blood disorders, while acquired mutations would be found associated with essentially all cases of acute megakaryoblastic leukemia (AMKL) in children with Down syndrome (DS). With respect to the latter disorder, the presence of a GATA1 mutation is now arguably the defining feature of this leukemia. In this review, I will summarize our current knowledge of the role of GATA-1 in normal development, and discuss how mutations in GATA1 lead to abnormal and malignant hematopoiesis.

Original languageEnglish (US)
Pages (from-to)137-147
Number of pages11
JournalSeminars in Cell and Developmental Biology
Volume16
Issue number1
DOIs
StatePublished - Feb 2005

Keywords

  • Erythrocytes
  • GATA-1
  • Hematopoiesis
  • Leukemia
  • Megakaryocytes

ASJC Scopus subject areas

  • Developmental Biology
  • Cell Biology

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