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Yingzi Yang

Researcher at Harvard University

Publications -  99
Citations -  11414

Yingzi Yang is an academic researcher from Harvard University. The author has contributed to research in topics: Wnt signaling pathway & Hedgehog signaling pathway. The author has an hindex of 43, co-authored 91 publications receiving 9839 citations. Previous affiliations of Yingzi Yang include Memorial Sloan Kettering Cancer Center & Cornell University.

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Wnt/β-Catenin Signaling in Mesenchymal Progenitors Controls Osteoblast and Chondrocyte Differentiation during Vertebrate Skeletogenesis

TL;DR: The results demonstrate that beta-catenin is essential in determining whether mesenchymal progenitors will become osteoblasts or chondrocytes regardless of regional locations or ossification mechanisms.
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Wnt-5a inhibits the canonical Wnt pathway by promoting GSK-3–independent β-catenin degradation

TL;DR: A new noncanonical pathway through which Wnt-5a antagonizes the canonical Wnt pathway by promoting the degradation of β-catenin is uncovered.
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Genetic manipulation of hedgehog signaling in the endochondral skeleton reveals a direct role in the regulation of chondrocyte proliferation.

TL;DR: The present study establishes Ihh as a key mitogen in the endochondral skeleton by overexpressing either Ihh or a constitutively active Smo allele specifically in the cartilage using the bigenic UAS-Gal4 system, demonstrating that activation of the Ihh signaling pathway is sufficient to promote chondrocyte proliferation.
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Mammalian Mst1 and Mst2 kinases play essential roles in organ size control and tumor suppression

TL;DR: It is found that Mst1 and Mst2, the two mouse homologs of the Drosophila Hpo, control the sizes of some, but not all organs, in mice, and MSt1 andMst2 act as tumor suppressors by restricting cell proliferation and survival.
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Wnt Signaling Gradients Establish Planar Cell Polarity by Inducing Vangl2 Phosphorylation through Ror2

TL;DR: Wnt signaling gradient provides directional information to a field of cells and provides new insight to Robinow syndrome, Brachydactyly Type B1, and spinal bifida which are caused by mutations in human ROR2, WNT5A, or VANGL.