Shuying Yang
University of Pennsylvania
64 Papers
59 Citations
Shuying Yang is an academic researcher from University of Pennsylvania. The author has contributed to research in topics: Biology & Osteoclast. The author has an hindex of 21, co-authored 49 publications. Previous affiliations of Shuying Yang include The Forsyth Institute & University at Buffalo.
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Papers
Signaling and transcriptional regulation in osteoblast commitment and differentiation.
TL;DR: This review summarizes the recent advances in the studies of signaling transduction pathways and transcriptional regulation of osteoblast cell lineage commitment and differentiation that enable a better understanding of the multiple factors and signaling networks that control the differentiation process at a molecular level.
Bone marrow adipogenic lineage precursors promote osteoclastogenesis in bone remodeling and pathologic bone loss
Wei Yu,Wei Yu,Leilei Zhong,Lutian Yao,Yulong Wei,Yulong Wei,Tao Gui,Tao Gui,Ziqing Li,Hyunsoo Kim,Nicholas Holdreith,Nicholas Holdreith,Xi Jiang,Wei Tong,Wei Tong,Nathaniel A. Dyment,X. Sherry Liu,Shuying Yang,Yongwon Choi,Jaimo Ahn,Ling Qin +20 more
TL;DR: These studies identified MALPs as a critical player in controlling bone remodeling during normal bone metabolism and pathological bone loss in a RANKL-dependent fashion.
RGS10-null mutation impairs osteoclast differentiation resulting from the loss of [Ca2+]i oscillation regulation.
Shuying Yang,Yi-Ping Li +1 more
TL;DR: A mechanism through which R GS10 specifically regulates the RANKL-evoked RGS10/calmodulin-[Ca2+]i oscillation-calcineurin-NFATc1 signaling pathway in osteoclast differentiation is revealed using an in vivo model and provides a potential therapeutic target for the treatment of bone diseases.
Ciliary IFT80 balances canonical versus non-canonical hedgehog signalling for osteoblast differentiation
TL;DR: It is shown that deletion of ciliary IFT80 in OB precursor cells (OPC) in mice results in growth retardation and markedly decreased bone mass with impaired OB differentiation, and is highlighted as a therapeutic target for craniofacial and skeletal abnormalities.
Novel pycnodysostosis mouse model uncovers cathepsin K function as a potential regulator of osteoclast apoptosis and senescence
TL;DR: The results show that cathepsin K function has different effects around the skeleton due to site-specific variations in bone homeostasis, such as phenotypes of osteopetrosis in tibiae and osteolysis in calvariae as a result of cathePSin K mutation.
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