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Kyunghee Choi

Researcher at Washington University in St. Louis

Publications -  75
Citations -  4986

Kyunghee Choi is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Haematopoiesis & Embryonic stem cell. The author has an hindex of 35, co-authored 71 publications receiving 4599 citations. Previous affiliations of Kyunghee Choi include Kyung Hee University.

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Discovering hematopoietic mechanisms through genome-wide analysis of GATA factor chromatin occupancy.

TL;DR: Fundamental principles underlying GATA factor mechanisms in chromatin are established and a complex network of considerable importance for the control of hematopoiesis is illustrated.
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ER71 acts downstream of BMP, Notch, and Wnt signaling in blood and vessel progenitor specification.

TL;DR: It is shown that combined BMP, Notch, and Wnt signaling is necessary for efficient FLK1(+) mesoderm formation from embryonic stem cells (ESCs) andforced expression of ER71 in ESCs resulted in a robust induction of FLK 1(+) Mesoderm.
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Combinatorial effects of Flk1 and Tal1 on vascular and hematopoietic development in the mouse.

TL;DR: A model in which the combinatorial effects of Flk1 and Tal1 act to regulate cell fate choice in early development into hematopoietic, endothelial, and smooth muscle lineages is proposed.
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A hierarchical order of factors in the generation of FLK1- and SCL-expressing hematopoietic and endothelial progenitors from embryonic stem cells.

TL;DR: The studies suggest that hematopoietic and endothelial commitment from the mesoderm occurs via BMP4-mediated signals and that expansion and/or differentiation of such progenitors is achieved by an interplay of VEGF, TGFβ1 and activin A signaling.
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Fibroblast growth factor signals regulate a wave of Hedgehog activation that is essential for coronary vascular development

TL;DR: It is demonstrated that HH is necessary for coronary vascular development and activation of HH signaling is sufficient to promote coronary growth and to rescue coronary defects due to loss of FGF signaling, which implicate HH signaling as an essential regulator of coronary vascularDevelopment and as a potential therapeutic target for coronary neovascularization.