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Honggang Ye

Researcher at University of Chicago

Publications -  38
Citations -  2284

Honggang Ye is an academic researcher from University of Chicago. The author has contributed to research in topics: Adipose tissue & Adipocyte. The author has an hindex of 21, co-authored 35 publications receiving 2015 citations. Previous affiliations of Honggang Ye include Howard Hughes Medical Institute.

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Insulin gene mutations as a cause of permanent neonatal diabetes

TL;DR: Ten heterozygous mutations in the human insulin gene are reported in 16 probands with neonatal diabetes, and it is predicted that they prevent normal folding and progression of proinsulin in the insulin secretory pathway.
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Involvement of the vitamin D receptor in energy metabolism: regulation of uncoupling proteins

TL;DR: The metabolic phenotypes of vitamin D receptor (VDR)-null mutant mice are characterized and data indicate that vitamin D is involved in energy metabolism and adipocyte biology in vivo in part through regulation of beta-oxidation and UCP expression.
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RyR2 and Calpain-10 Delineate a Novel Apoptosis Pathway in Pancreatic Islets

TL;DR: It is demonstrated that the calpain-10 isoform mediated ryanodine-induced apoptosis, a type 2 diabetes susceptibility gene with previously unknown function, and RyR2 activity seems to play an essential role in β-cell survival in vitro by suppressing a death pathway mediated by cal pain-10.
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Targeted Expression of Human Vitamin D Receptor in Adipocytes Decreases Energy Expenditure and Induces Obesity in Mice

TL;DR: An important role of the VDR in the regulation of energy metabolism is confirmed after a transgenic approach used the aP2 gene promoter to target the expression of the human (h)VDR in adipocytes in mice to further define the role of V DR in adipocyte biology.
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Alterations in TCF7L2 expression define its role as a key regulator of glucose metabolism

TL;DR: Results directly demonstrate that Tcf7l2 plays a role in regulating glucose tolerance, suggesting that overexpression of this gene is associated with increased risk of T2D, strengthening the evidence that variation in cis-regulatory elements may be a paradigm for genetic predispositions to common disease.