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Yingqun Huang on Muck Rack

Yingqun Huang

As seen in: Nature, Cell Press, The Journal of Clinical Investigation
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Articles

TET3-overexpressing macrophages are a unifying pathogenic feature with therapeutic potential in chronic inflammatory diseases

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By Yoshihiro Ogawa, Beibei Liu, Yingqun Huang, Shojiro Haji
| The Journal of Clinical Investigation
Abstract Increased activation of the NLRP3 inflammasome in immune cells, including macrophages, has been implicated in the pathogenesis of multiple chronic inflammatory diseases. Targeted depletion of macrophages has been explored as a cross-disease therapeutic strategy, but without subtype-specific markers, this strategy risks elimination of macrophages with homeostatic functions. In this study, Liu et al.
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Regulated circRNA nuclear export in neuronal differentiation

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By Yingqun Huang
| Cell Press Verified
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Hepatic TET3 contributes to type-2 diabetes by inducing the HNF4α fetal isoform

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By Xiaoyong Yang, Sabrina Diano, Gordon G. Carmichael, Yingqun Huang
| Nature Verified
Abstract Precise control of hepatic glucose production (HGP) is pivotal to maintain systemic glucose homeostasis. HNF4α functions to stimulate transcription of key gluconeogenic genes. HNF4α harbors two promoters (P2 and P1) thought to be primarily active in fetal and adult livers, respectively. Here we report that the fetal version of HNF4α is required for HGP in the adult liver. This isoform is acutely induced upon fasting and chronically increased in type-2 diabetes (T2D).
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