The role of PU.1 and GATA-1 transcription factors during normal and leukemogenic hematopoiesis

• Published in: Leukemia Vol. 24; no. 7; pp. 1249 - 1257
• Main Authors: Burda, P, Laslo, P, Stopka, T
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 01-07-2010; Nature Publishing Group
• Subjects: 631/250/232; 631/67/1990/283; 631/92/612/822; Animals; Binding sites; Biological and medical sciences; Cancer Research; Cell differentiation; Cell fate; Critical Care Medicine; Differentiation (biology); GATA Transcription Factors - physiology; Gene expression; Genetic aspects; Genetic regulation; Hematologic and hematopoietic diseases; Hematology; Hematopoiesis; Hematopoiesis - physiology; Humans; Intensive; Internal Medicine; Leukemia; Leukemia - metabolism; Leukemia - pathology; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis; Medical sciences; Medicine; Medicine & Public Health; Oncology; Physiological aspects; Protein interaction; Proteins; Proto-Oncogene Proteins - physiology; PU.1 protein; review; Stem cells; Trans-Activators - physiology; Transcription factors; Czech Republic; GATA-1; chromatin; differentiation therapy; leukemia differentiation; PU.1; Chromatin; Hematology; Leukemia; Malignant hemopathy; Cell differentiation; Signal transduction; Transcription factor PU.1; Hematopoiesis; Transcription factor; Transcription factor GATA1; Cancer
• ISSN: 0887-6924; 1476-5551
• DOI: 10.1038/leu.2010.104

Hematopoiesis is coordinated by a complex regulatory network of transcription factors and among them PU.1 (Spi1, Sfpi1) represents a key molecule. This review summarizes the indispensable requirement of PU.1 during hematopoietic cell fate decisions and how the function of PU.1 can be modulated by protein–protein interactions with additional factors. The mutual negative regulation between PU.1 and GATA-1 is detailed within the context of normal and leukemogenic hematopoiesis and the concept of ‘differentiation therapy’ to restore normal cellular differentiation of leukemic cells is discussed.