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Stuart Smith

Researcher at Children's Hospital Oakland Research Institute

Publications -  75
Citations -  6640

Stuart Smith is an academic researcher from Children's Hospital Oakland Research Institute. The author has contributed to research in topics: Fatty acid synthase & Acyl carrier protein. The author has an hindex of 40, co-authored 75 publications receiving 6328 citations. Previous affiliations of Stuart Smith include University of California, San Francisco.

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Crystal structure of the Escherichia coli thioesterase II, a homolog of the human Nef binding enzyme.

TL;DR: The structure of the E. coli thioesterase II reveals a new tertiary fold, a ‘double hot dog’, showing an internal repeat with a basic unit that is structurally similar to the recently described β-hydroxydecanoyl thiol ester dehydrase.
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Neurogenin3 and Hepatic Nuclear Factor 1 Cooperate in Activating Pancreatic Expression of Pax4

TL;DR: It is demonstrated how Neurogenin3 and HNF1α activate the pax4 gene during the cascade of gene expression events that control pancreatic endocrine cell development.
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Hedgehog signaling regulates expansion of pancreatic epithelial cells.

TL;DR: Ectopically activate the Hedgehog pathway midway through pancreas development via expression of either Sonic (Shh) or Indian Hedgehog (Ihh) under control of the human Pax4-promoter, showing that Hedgehog signaling controls mesenchymal vs. epithelial tissue differentiation and that pathway activation impairs formation of epithelial progenitors.
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Insulin acutely decreases hepatic fatty acid synthase activity.

TL;DR: Failure of insulin to acutely reduce hepatic FAS activity in hyperinsulinemic mice, including L-SACC1 transgenics with liver inactivation of CEACAM1, and Ob/Ob obese mice, suggests that the acute effect of insulin on FAS action depends on the prior insulinemic state.
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PAX4 gene variations predispose to ketosis-prone diabetes

TL;DR: Data provide the first evidence that ethnic-specific gene variants may contribute to the predisposition to this particular form of diabetes and suggest that KPD, like maturity onset diabetes of the young, is a rare, phenotypically defined but genetically heterogeneous form of type 2 diabetes.