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Keiichiro Hiratsu

Researcher at National Institute of Advanced Industrial Science and Technology

Publications -  36
Citations -  4577

Keiichiro Hiratsu is an academic researcher from National Institute of Advanced Industrial Science and Technology. The author has contributed to research in topics: Transcription factor & Gene. The author has an hindex of 15, co-authored 36 publications receiving 4124 citations. Previous affiliations of Keiichiro Hiratsu include National Defense Academy of Japan.

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AREB1 Is a Transcription Activator of Novel ABRE-Dependent ABA Signaling That Enhances Drought Stress Tolerance in Arabidopsis

TL;DR: It is shown that expression of the intact AREB1 gene on its own is insufficient to lead to expression of downstream genes under normal growth conditions, and data suggest that AREB 1 regulates novel ABRE-dependent ABA signaling that enhances drought tolerance in vegetative tissues.
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Repression Domains of Class II ERF Transcriptional Repressors Share an Essential Motif for Active Repression

TL;DR: Analysis of the results of a series of deletions revealed that the C-terminal 35 amino acids of NtERF3 are sufficient to confer the capacity for repression of transcription on a heterologous DNA binding domain, and this repression domain suppressed the intermolecular activities of other transcriptional activators.
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Dominant repression of target genes by chimeric repressors that include the EAR motif, a repression domain, in Arabidopsis.

TL;DR: It is shown that four different transcription factors fused to the EAR motif act as dominant repressors in transgenic Arabidopsis and suppress the expression of specific target genes, even in the presence of the redundant transcription factors, with resultant dominant loss-of-function phenotypes.
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The AP2/ERF Transcription Factor WIND1 Controls Cell Dedifferentiation in Arabidopsis

TL;DR: Novel molecular insights are provided into how plants control cell dedifferentiation in response to wounding by demonstrating that wounding upregulates the B-type ARABIDOPSIS RESPONSE REGULATOR (ARR)-mediated cytokinin response and that WIND1 acts via the ARR-dependent signaling pathway to promote cell ded indifferentiation.