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Regulation of GATA1 Gene Expression

Authors: Makoto, Kobayashi; Masayuki, Yamamoto;

Regulation of GATA1 Gene Expression

Abstract

GATA1 is one of the most fascinating transcription factors for biologists. It regulates many haematopoietic genes and interacts with a number of other transcription factors. Its functions are mostly conserved among vertebrates. Upon disruption of the GATA1 gene, mice show a drastic bloodless phenotype. GATA1 knockdown mice are predisposed to tumour development, the extent of which varies depending on the level of knockdown. When GATA1 is overexpressed, certain cells face an altered cell fate. These observations suggest the importance of regulation on the expression level and timing of GATA1. Deciphering such regulation is the key to understanding the commitment and differentiation of blood cells. There are so many splendid reviews describing GATA1 as a transcription factor. We therefore focus our topics on GATA1 gene regulation in this review.

Keywords

Mice, Gene Expression Regulation, Gene Expression Profiling, Trans-Activators, Animals, Humans, Cell Differentiation, GATA1 Transcription Factor, Regulatory Elements, Transcriptional, Models, Biological

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Powered by OpenAIRE graph
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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
29
Top 10%
Average
Top 10%
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