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James D. Johnson

Researcher at University of British Columbia

Publications -  201
Citations -  15036

James D. Johnson is an academic researcher from University of British Columbia. The author has contributed to research in topics: Insulin & Insulin resistance. The author has an hindex of 49, co-authored 186 publications receiving 13078 citations. Previous affiliations of James D. Johnson include Vancouver General Hospital & University of Alberta.

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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Reversal of diabetes with insulin-producing cells derived in vitro from human pluripotent stem cells

Alireza Rezania, +12 more
- 01 Nov 2014 - 
TL;DR: Although S7 cells are not fully equivalent to mature beta cells, their capacity for glucose-responsive insulin secretion and rapid reversal of diabetes in vivo makes them a promising alternative to pancreatic progenitor cells or cadaveric islets for the treatment of diabetes.
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Hyperinsulinemia Drives Diet-Induced Obesity Independently of Brain Insulin Production

Arya E. Mehran, +12 more
- 05 Dec 2012 - 
TL;DR: Genetic evidence that pathological circulating hyperinsulinemia drives diet-induced obesity and its complications is provided and white adipose tissue is reprogrammed to express uncoupling protein 1 and increase energy expenditure.
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Beta-cell ABCA1 influences insulin secretion, glucose homeostasis and response to thiazolidinedione treatment.

Liam R. Brunham, +11 more
- 01 Mar 2007 - 
TL;DR: A new role for Abca1 is established in β-cell cholesterol homeostasis and insulin secretion, and it is suggested that cholesterol accumulation may contribute to β- cell dysfunction in type 2 diabetes.
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Increased islet apoptosis in Pdx1+/- mice

James D. Johnson, +8 more
- 15 Apr 2003 - 
TL;DR: An increase in apoptosis, with abnormal regulation of islet number and beta cell mass, represents a key mechanism whereby partial PDX1 deficiency leads to an organ-level defect in insulin secretion and diabetes.