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James Johnson - Diabetes Canada. Vancouver, BC, CA

James Johnson James Johnson

Professor, LSI Diabetes Research Group | Diabetes Canada

Vancouver, BC, CANADA

Professor in Cellular & Physiological Sciences and Surgery and Diabetes Research Group Leader at the University of British Columbia

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UBC Killam Profile 2014 James Johnson

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Biography

Dr. Johnson is a Full Professor in the Department of Cellular and Physiological Sciences, in the Faculty of Medicine at the University of British Columbia. He is Leader of the Life Sciences Institute Diabetes Research Group, consisting of 8 laboratories and >70 staff/trainees.

He is also helping to start up and direct a new academic-industry hybrid type 2 diabetes research institute in Oxford funded by Novo Nordisk. He will do this while maintaining his academic laboratory at UBC.

His research group at UBC studies the pathophysiology and signalling mechanisms underlying diabetes, obesity, longevity, heart disease, Alzheimer's disease and pancreatic cancer. He is Editor-in-Chief of Islets and serves on the Editorial Boards of Diabetes and of Endocrinology.

Industry Expertise (4)

Education/Learning Health and Wellness Research Training and Development

Areas of Expertise (5)

Cell Biology Diabetes Molecular Biology Biochemistry Cell Culture

Accomplishments (6)

2016 Diabetes Canada Young Scientist Award (professional)

2016-10-28

Diabetes Canada established the Young Scientist Award in 1987 for the purpose of encouraging, by appropriate recognition, outstanding research conducted in Canada by young scientists in the field of diabetes. This award continues today with the support of the CH Best Research Fund of Canadian Diabetes Association.

Visiting Scholar – Harris Manchester College, Oxford University (professional)

2014

Visiting Professor of Integrated Physiology, Oxford University (personal)

2014-2017

Killam Research Fellowship (professional)

2014

Researcher of the Year, Department of Cellular and Physiological Sciences, University of British Columbia (professional)

2009

Murray L Barr Award, Canadian Association for Anatomy Neurobiology and Cell Biology (professional)

2007

Education (4)

Washington University Medical Cente: Post-doctoral Fellowship 2004

Washington University School of Medicine: Fellow of the Lucille P. Markey Pathway, Human Pathobiology 2003

University of Alberta: Ph.D., Physiology and Cell Biology 2000

Lakehead University: HBKin, Kinesiology 1996

Affiliations (1)

  • Professor LSI Diabetes Research Group University of British Columbia

Articles (5)

Carboxypeptidase E mediates palmitate-induced beta-cell ER stress and apoptosis. PNAS

2008-06-17

Obesity is a principal risk factor for type 2 diabetes, and elevated fatty acids reduce beta-cell function and survival. An unbiased proteomic screen was used to identify targets of palmitate in beta-cell death. The most significantly altered protein in both human islets and MIN6 beta-cells treated with palmitate was carboxypeptidase E (CPE). Palmitate reduced CPE protein levels within 2 h, preceding endoplasmic reticulum (ER) stress and cell death, by a mechanism involving CPE translocation to Golgi and lysosomal degradation. Palmitate metabolism and Ca(2+) flux were also required for CPE proteolysis and beta-cell death. Chronic palmitate exposure increased the ratio of proinsulin to insulin. CPE null islets had increased apoptosis in vivo and in vitro. Reducing CPE by approximately 30% using shRNA also increased ER stress and apoptosis. Conversely, overexpression of CPE partially rescued beta-cells from palmitate-induced ER stress and apoptosis. Thus, carboxypeptidase E degradation contributes to palmitate-induced beta-cell ER stress and apoptosis. CPE is a major link between hyperlipidemia and beta-cell death pathways in diabetes.

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Hyperinsulinemia Drives Diet-Induced Obesity Independently of Brain Insulin Production Cell Metabolism

2012-12-05

Insulin 2 (INSULIN), but not Insulin 1, is produced locally in the adult brain; circulating insulin can be reduced without sustained changes in glucose homeostasi; fasting hyperinsulinemia is required for diet-induced obesity and its complications; insulin controls Ucp1 in white adipose tissue and energy expenditure

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Suppression of hyperinsulinaemia in growing female mice provides long-term protection against obesity Diabetologia

2015

Hyperinsulinaemia is associated with obesity but its causal role in the onset of obesity remains controversial. In this study, we tested the hypothesis that transient attenuation of diet-induced insulin hypersecretion in young mice can provide sustained protection against obesity throughout adult life...

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14-3-3z coordinates visceral fat adipogenesis Nature Communications

2015

The proteins that coordinate complex adipogenic transcriptional networks are poorly understood. 14-3-3ζ is a molecular adaptor protein that regulates insulin signalling and transcription factor networks. Here we report that 14-3-3ζ-knockout mice are strikingly lean from birth with specific reductions in visceral fat depots. Conversely, transgenic 14-3-3ζ overexpression potentiates obesity, without exacerbating metabolic complications...

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A live-cell, high-content imaging survey of 206 biologic factors across 5 stress conditions reveals context dependent survival effects in primary beta-cells Diabetologia

2015

Beta cell death is a hallmark of diabetes. It is not known whether specific cellular stresses associated with type 1 or type 2 diabetes require specific factors to protect pancreatic beta cells. No systematic comparison of endogenous soluble factors in the context of multiple pro-apoptotic conditions has been published...

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