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Fenglei He

Researcher at Tulane University

Publications -  30
Citations -  1428

Fenglei He is an academic researcher from Tulane University. The author has contributed to research in topics: Neural crest & Wnt signaling pathway. The author has an hindex of 17, co-authored 27 publications receiving 1247 citations. Previous affiliations of Fenglei He include Ohio State University & Icahn School of Medicine at Mount Sinai.

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Wnt5a regulates directional cell migration and cell proliferation via Ror2-mediated noncanonical pathway in mammalian palate development.

TL;DR: This work shows that Wnt5a and its receptor Ror2 are expressed in a graded manner along the AP axis of the palate, and reveals distinct regulatory roles for Wnt 5a in gene expression and cell proliferation and an essential role in the regulation of directional cell migration within the developing palate.
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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.
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Control of hair follicle cell fate by underlying mesenchyme through a CSL–Wnt5a–FoxN1 regulatory axis

TL;DR: It is reported that maintenance of the hair follicle keratinocyte cell fate is defective in mice with mesenchymal deletion of the CSL/RBP-Jkappa gene, the effector of "canonical" Notch signaling.
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Modulation of BMP signaling by Noggin is required for the maintenance of palatal epithelial integrity during palatogenesis.

TL;DR: It is concluded that Noggin mediated modulation of BMP signaling is essential for palatal epithelium integrity and for normal palate development.
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Wnt5a regulates growth, patterning, and odontoblast differentiation of developing mouse tooth

TL;DR: It is suggested that Wnt5a regulates growth, patterning, and odontoblast differentiation during odontogenesis, at least partially by modulating Wnt/β‐catenin canonical signaling.