Unsuspected role for the T-cell leukemia protein SCL/tal-1 in vascular development
Article Abstract:
SCL/tal-1, transcription factor, is needed for blood cell development. Transgenic rescue of hematopoietic defects of SCL-/- embryos and study of chimeras generated with SCL-/- ES cells tagged with a transgene in vascular endothelial cells have been used to show that SCL is needed for angiogenesis reforming of the yolk sac capillary network into a complex network of vitelline vessels. SCL is a factor in embryonic angiogenesis. It seems to have vital functions in both embryonic blood and vascular cells, descendents of the presumptive hemangioblast. T-cell leukemia protein SCL/tal-1 in vascular development has an unexpected role in vascular development.
Publication Name: Genes & Development
Subject: Biological sciences
ISSN: 0890-9369
Year: 1998
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FOG, a multitype zinc finger protein, acts as a cofactor for transcription factor GATA-1 in erythroid and megakaryotic differentiation
Article Abstract:
The binding properties of GATA-1 was analyzed by utilizing the conserved zinc-finger DNA-binding domain of the hematopoietic transcription factor. Analysis of the primary polypeptide sequence of GATA-1 indicated the presence of a nuclear zinc-finger protein termed Friend of GATA-1 or FOG which acted as a GATA-1 cofactor. Furthermore, FOG and GATA-1 were coexpressed during embryonic and hematopoietic development and theysynergistically activated transcription from a hematopoietic-specific regulatory region.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1997
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The TEL/ETV6 gene is required specifically for hematopoiesis in the bone marrow
Article Abstract:
The translocation-Ets-leukemia (TEL) or ETV6 locus encodes an Ets family transcription factor. It is often changed in human leukemias with myeloid/lymphoid origins. The gene is necessary for hematopoiesis in bone marrow. TEL is the first transcription factor found to be necessary for this. It has a vital role in the normal shift of hematopoietic activity from fetal liver to bone marrow.
Publication Name: Genes & Development
Subject: Biological sciences
ISSN: 0890-9369
Year: 1998
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