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Sona Kang

Researcher at University of California, Berkeley

Publications -  37
Citations -  2547

Sona Kang is an academic researcher from University of California, Berkeley. The author has contributed to research in topics: Adipose tissue & Insulin resistance. The author has an hindex of 20, co-authored 35 publications receiving 2170 citations. Previous affiliations of Sona Kang include Chonnam National University & Harvard University.

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Wnt Signaling Stimulates Osteoblastogenesis of Mesenchymal Precursors by Suppressing CCAAT/Enhancer-binding Protein α and Peroxisome Proliferator-activated Receptor γ

TL;DR: It is demonstrated that transient activation of Wnt/β-catenin signaling rapidly suppresses C/EBPα and PPARγ, followed by activation of osteoblastogenic transcription factors, suggesting that Wnt signaling alters the fate of mesenchymal precursor cells primarily by suppressing C/Wntα andPPARγ.
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Wnt10b inhibits development of white and brown adipose tissues.

TL;DR: Inhibition by Wnt10b of white and brown adipose tissue development results in lean mice without lipodystrophic diabetes.
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IRF4 Is a Key Thermogenic Transcriptional Partner of PGC-1α

TL;DR: Interferon regulatory factor 4 is identified as a dominant transcriptional effector of thermogenesis and induced by cold and cAMP in adipocytes and is sufficient to promote increased thermogenic gene expression, energy expenditure, and cold tolerance.
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Role of wnts in prostate cancer bone metastases

TL;DR: This model suggests that targeting both osteolytic activity and osteoblastic activity will provide efficacy for therapy of CaP bone metastases, and it is believed that DKK‐1 is one of the switches that transitions the CaPBone metastasis activity from osteolyic to osteobastic.
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Wnt10b inhibits obesity in ob/ob and agouti mice

TL;DR: In this paper, the Wnt family of secreted signaling molecules has profound effects on diverse developmental processes, including the fate of mesenchymal progenitors, and it is shown that Wnt signaling blocks adipogenesis and promotes spontaneous preadipocyte differentiation.