B
Barbara E. Corkey
Researcher at Boston University
Publications - 198
Citations - 18473
Barbara E. Corkey is an academic researcher from Boston University. The author has contributed to research in topics: Insulin & Glycolysis. The author has an hindex of 72, co-authored 194 publications receiving 17071 citations. Previous affiliations of Barbara E. Corkey include Brigham and Women's Hospital & Upjohn.
Papers
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Journal ArticleDOI
Fission and selective fusion govern mitochondrial segregation and elimination by autophagy
Gilad Twig,Alvaro A. Elorza,Anthony J.A. Molina,Anthony J.A. Molina,Hibo Mohamed,Jakob D. Wikstrom,Gil Walzer,Linsey Stiles,Sarah E. Haigh,Steve Katz,Guy Las,Joseph Alroy,Min Wu,Bénédicte F. Py,Junying Yuan,Jude T. Deeney,Barbara E. Corkey,Orian S. Shirihai +17 more
TL;DR: Pulse chase and arrest of autophagy at the pre‐proteolysis stage reveal that fission followed by selective fusion segregates dysfunctional mitochondria and permits their removal by autophagic.
Book ChapterDOI
[65] Assays of intermediates of the citric acid cycle and related compounds by fluorometric enzyme methods
TL;DR: This chapter is based on the assays of intermediates of the citric acid cycle and related compounds by fluorometric enzyme methods based on instruments capable of giving a full-scale deflection of the recorder with 0.25μM NADH, with a noise level less than 2%.
Journal ArticleDOI
Reactive Oxygen Species as a Signal in Glucose-Stimulated Insulin Secretion
Jingbo Pi,Yushi Bai,Qiang Zhang,Victoria A. Wong,Lisa M. Floering,Kiefer W. Daniel,Jeffrey M. Reece,Jude T. Deeney,Melvin E. Andersen,Barbara E. Corkey,Sheila Collins +10 more
TL;DR: Findings suggest that H2O2 derived from glucose metabolism is one of the metabolic signals for insulin secretion, whereas oxidative stress may disturb its signaling function.
Journal ArticleDOI
Are the beta-cell signaling molecules malonyl-CoA and cystolic long-chain acyl-CoA implicated in multiple tissue defects of obesity and NIDDM?
M Prentki,Barbara E. Corkey +1 more
TL;DR: If the hypothesis is correct that common signaling abnormalities in the metabolism of malonyl-CoA and LC- CoA contribute to altered insulin release and sensitivity, it offers a novel explanation for the presence of variable combinations of these defects in individuals with differing genetic backgrounds.
Journal ArticleDOI
Malonyl-CoA and long chain acyl-CoA esters as metabolic coupling factors in nutrient-induced insulin secretion.
TL;DR: Data provide further support for a model in which malonyl-CoA and long chain acyl-CoAs esters serve as metabolic coupling factors when pancreatic beta-cells are stimulated with glucose and other nutrient secretagogues.