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YiPing Chen

Researcher at Tulane University

Publications -  91
Citations -  5139

YiPing Chen is an academic researcher from Tulane University. The author has contributed to research in topics: Mesenchyme & Sonic hedgehog. The author has an hindex of 37, co-authored 80 publications receiving 4675 citations. Previous affiliations of YiPing Chen include Fujian Normal University & Brigham and Women's Hospital.

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Msx1 controls inductive signaling in mammalian tooth morphogenesis

TL;DR: It is demonstrated that Msx1 is not only expressed in dental mesenchyme in response to epithelial signals, but also in turn regulates the reciprocal expression of inductive signals in the mesenchYme which then act back upon the dental epithelium.
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Rescue of cleft palate in Msx1-deficient mice by transgenic Bmp4 reveals a network of BMP and Shh signaling in the regulation of mammalian palatogenesis.

TL;DR: Msx1 controls a genetic hierarchy involving BMP and Shh signals that regulates the growth of the anterior region of palate during mammalian palatogenesis and provides insights into the cellular and molecular etiology of the non-syndromic clefting associated with Msx1 mutations.
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Making a tooth: growth factors, transcription factors, and stem cells.

TL;DR: For instance, this paper showed that stem cells are highly plastic and multipotent and could be reprogrammed into odontogenic fate and participated in tooth formation. But, the development of human tooth is largely dependent on sequential and reciprocal epithelial-mesenchymal interactions.
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Msx homeobox gene family and craniofacial development.

TL;DR: This review summarizes studies on the expression, regulation, and functional analysis of Msx genes that bear relevance to craniofacial development in humans and mice.
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Shox2 is essential for the differentiation of cardiac pacemaker cells by repressing Nkx2-5

TL;DR: It is demonstrated that Shox2 plays an essential role in the SAN and pacemaker development by controlling a genetic cascade through the repression of Nkx2-5 in the developing heart, leading to a reduced cardiac field and aberrant heart formation.