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Robert V. Farese
Researcher at Harvard University
Publications - 484
Citations - 54181
Robert V. Farese is an academic researcher from Harvard University. The author has contributed to research in topics: Insulin & Protein kinase C. The author has an hindex of 115, co-authored 473 publications receiving 48754 citations. Previous affiliations of Robert V. Farese include University of South Florida & University at Buffalo.
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Journal ArticleDOI
On the mechanism whereby ACTH and cyclic AMP increase adrenal polyphosphoinositides. Rapid stimulation of the synthesis of phosphatidic acid and derivatives of CDP - diacylglycerol.
TL;DR: The results suggest that the ACTH-induced increase in polyphosphoinositides is due to a rapid increase in phosphatidic acid and, subsequently, CDP-diacylglycerol andosphatidylinositol.
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PKC-ζ Mediates Insulin Effects on Glucose Transport in Cultured Preadipocyte-Derived Human Adipocytes
Gautam Bandyopadhyay,Mini P. Sajan,Yoshinori Kanoh,Mary L. Standaert,Michael J. Quon,Rene Lea-Currie,Anindita Sen,Robert V. Farese +7 more
TL;DR: These findings provide convincing evidence that aPKCs and upstream activators, PI 3-kinase and PDK-1, play important roles in insulin-stimulated glucose transport in preadipocyte-derived human adipocytes.
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Progranulin: at the interface of neurodegenerative and metabolic diseases
TL;DR: Progranulin biology in both neurodegenerative and metabolic diseases is reviewed, highlighting the growth factor-like, trophic, and anti-inflammatory properties of progranulin as potential unifying themes in these seemingly divergent conditions.
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Polyphosphoinositides:stimulator of mitochondrial cholesterol side chain cleavage and possible identification as an adrenocorticotropin-induced, cycloheximide-sensitive, cytosolic, steroidogenic factor.
Robert V. Farese,Ayub M. Sabir +1 more
TL;DR: Findings from the laboratory suggest that polyphosphoinositides may function as a cycloheximide-sensitive mediator in the steroidogenic action of ACTH.
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Analysis of energy expenditure at different ambient temperatures in mice lacking DGAT1
TL;DR: The results suggest that the hyperphagia in Dgat1(-/-) mice is a secondary mechanism that compensates for the increased utilization of fuel substrates and increased energy expenditure in a murine model of obesity resistance.