James Johnson, Professor

LSI Diabetes Research Group
LSI Cardiovascular Research Group

Laboratory of Molecular Signalling in Diabetes
5358 – 2350 Health Sciences Mall, University of British Columbia
Vancouver, BC Canada V6T 1Z3

Office: 604-822-7187, Fax: 604-822-2316
Click here to access Dr. Johnson’s page on the Diabetes Research Group website

A b o u t   t h e   P I


PhD Cell Biology and Physiology, University of Alberta

Post-Doctoral Fellowship, Washington University Medical Center

Current Position

Professor, Cellular & Physiological Sciences and Surgery, University of British Columbia

Major Awards

2014 Killam Research Fellowship
2009 Researcher of the Year – Department of Cellular and Physiological Sciences
2008 UBC Faculty of Medicine Distinguished Achievement Award for Excellence in Basic Science Research
2007 Murray L Barr Award, Canadian Association for Anatomy Neurobiology and Cell Biology
2006 Canadian Diabetes Association Scholarship (declined)
2006 Canadian Institute of Health Research New Principal Investigator Award
2005 Juvenile Diabetes Research Foundation Career Development Award

P r o j e c t s

Causal Roles of Hyperinsulinemia in Obesity and Altered Longevity

The epidemics of obesity, type 2 diabetes and related diseases threaten to overrun the global healthcare system. We know that obesity, insulin resistance, early type 2 diabetes are all highly correlated with each other and are all associated with a higher than normal release of insulin from the pancreas, but we still do not fully understand the causal relationship between these phenomena. The most commonly accepted view is that obesity first leads to insulin resistance, which then leads to a compensatory hypersecretion of insulin, which finally results in diabetes when insulin release from the pancreas fail to meet demands. However, these implied cause and effect relationships have been questioned and are impossible to formally test in humans using rigorous genetic loss-of-function approaches. Indeed, there has long been evidence that basal insulin hypersecretion can precede insulin resistance and even obesity and clinical studies have also pointed to anti-obesity effects of drugs that block insulin secretion. We are testing the hypothesis that pancreatic insulin causes obesity directly, by genetically eliminating half of the insulin gene from the pancreas. We expect our study to have an important impact on our fundamental understanding of obesity, which might change the way we diagnose and treat millions of people. This work is funded by the Canadian Institutes of Health Research.
Roles of Brain-Produced Insulin in Alzheimer’s Disease

Many previous reports have suggested that small amounts of insulin may be produced locally by adult central neurons of mammals, including humans. Johnson’s group has recently confirmed these reports using rigorous negative and positive controls, but the function of centrally produced insulin remains a mystery. In this project, we will selectively delete the insulin 2 gene from the mouse brain in order to determine the role of central insulin. Previous studies have suggested that brain insulin is reduced in Alzheimer’s disease, making these studies highly relevant to human disease. This work is funded by the Alzheimer’s Society of Canada.

Hyperinsulinemia and Insulin Signalling in Pancreatic Cancer

Pancreatic adenocarcinoma is the fourth most common cause of cancer death in Canada, but receives the lowest proportion of research funding of any major cancer. As a result, our understanding of the factors that initiate and drive the progression of this disease remains poor relative to our knowledge pertaining to other cancers. Diabetes mellitus and obesity are emerging as important risk factors for pancreatic cancer and the rapid rise in BMI foreshadows a rise in pancreatic cancer. Elevated insulin levels are a feature of both obesity and type 2 diabetes. Hyperinsulinemia has been investigated as a possible contributor to cancer initiation and progression. Lowering hyperinsulinemia with metformin was shown to reduce the risk of pancreatic cancer by 60%. Groups in Europe created headlines worldwide by showing an increased risk of cancer with use of long-acting insulin analogues. The question of whether elevated insulin can be a causal in the pathogenesis of pancreatic cancer has not been rigorously tested. To test this hypothesis, we have established models engineered to lack multiple alleles of their two Insulin genes. Mice with two of four Insulin alleles are hyperinsulinemic on a high-fat diet, whereas mice lacking all but one Insulin allele are hypoinsulinemic but not diabetic. We also have mouse models that will allow us to test whether genes involved in insulin-stimulated proliferation and anti-apoptosis in pancreatic islets, Raf-1, Akt or Pdx-1, participate in pancreatic cancer. Whether insulin signalling might synergize with Kras, the most frequently mutated gene in pancreatic cancer, is a key unanswered question. The overall goal is to test the hypothesis that hyperinsulinemia in diabetes can contribute to hyperproliferation in the exocrine pancreas, promote pre-cancerous lesions, and promote the survival of pancreatic cancer cells. We will also test the hypothesis that Raf-1, Akt and Pdx-1 are critical for insulin action in the pancreas. Together, these studies have the potential to increase our understanding of this devastating disease and increase avenues towards rational therapeutic intervention. This information will eventually be used to identify novel compounds capable of blocking the hyperproliferative and anti-apoptotic effects of insulin in primary human pancreatic tissue and pancreatic tumor cell lines. This work has been funded by the Cancer Research Society of Canada.

Insulin Receptor Trafficking and Insulin ‘Feedback’ Signalling in Type 1 and Type 2 Diabetes

Insulin is both a metabolic hormone and growth factor. The signal transduction cascades activated by insulin have been well studied in ‘insulin target tissues’ such as muscle and fat. However, many studies have revealed unexpected tissues where blocking insulin signalling has adverse consequences to glucose homeostasis. Surprisingly, along with the liver and brain, these studies show that the pancreatic beta-cell itself an important site of insulin action. In addition, islets from human type 2 diabetics appear to be ‘insulin resistant’. We have investigated the role and mechanism of insulin signalling in the beta-cell and we have uncovered exciting differences compared to other tissues. We are continuing to study the effects of insulin on primary human and mouse islets, focusing on the anti-apoptotic effects of insulin and the mechanism of these effects. We have focused on signalling pathways regulated by the Raf-1 kinase and related proteins. We are testing the hypothesis that altered insulin expression plays a role in type 1 diabetes. Recently, we have developed a new way of following the movements of functional insulin receptors in living cells, and used this technology to make insights into insulin signal transduction. This project has been supported by grants from the Juvenile Diabetes Research Foundation and the Canadian Institute for Health Research.

High-Content Screening for Molecules that Promote Beta-Cell Survival

Virtually any cure for type 1 diabetes will require strategies to protect beta-cells from death and dysfunction. With recent support from JDRF, they have optimized novel imaging technologies that allow for the first time the simultaneous, real-time analysis beta-cell function and programmed cell death, on a single-cell basis. At the same time, using bioinformatics and genomics, our laboratory has compiled and published a list of 234 locally produced secreted factors and 233 secreted factor receptors. High-throughput screening approaches now make it possible to examine simultaneously all of these potential survival and differentiation factors under multiple conditions related to the pathogenesis of type 1 diabetes. The overall goal of the proposed study is to identify the most powerful locally acting survival and/or differentiation factors in human islets. Such a factor could be harnessed to improve graft survival in clinical islet transplantation, improve the production surrogate beta-cells, and eventually treat patients with type 1 diabetes and/or their at-risk family members. This work has been funded by the JDRF.

High-Content Screening for Molecules that Regulate Beta-Cell Differentiation Status

A major goal of regenerative medicine is the generation of fully functional pancreatic beta-cells, either from residual beta-cells in the patient or from stem cells. Both of these therapeutic avenues require a thorough understanding of the process by which beta-cells go from being immature to fully functional beta-cells. With SCN support, we devised a method to examine the maturation of single beta-cells for the first time using powerful custom microscopes and state-of-the-art fluorescent markers. At the same time, we have built (using CFI funds) the infrastructure to perform these experiments in a massively parallel manner. In doing so, we have become one of Canada’s leading centres for image-based screening in the diabetes field. This work has been funded by the Stem Cell Network and the JDRF.

New Roles for RyR2-Mediated Calcium Flux in Cardiomyocyte Survival, Metabolism

Every heartbeat is composed of a complex cycle of highly orchestrated events. The cardiac ryanodine receptor calcium channel (RyR2) is central to this cycle, releasing calcium to cause heart muscle cell contraction with each heartbeat. Diseases such as arrhythmias and diabetic cardiomyopathy are associated with changes in RyR2 function. However, it has remained unclear whether the other cellular symptoms of these conditions are causes or consequences of the loss of RyR2 function. Working in other cell types, we have recently described unexpected roles for RyR2, namely the control of gene expression and cell survival. In this project we examine hearts with selective deletion of RyR2 calcium channels and determine which cellular functions are changed most directly as a result. These studies will provide new insight into the dysfunction and death of heart cells in disease.

Calcium-Dependent Signal Transduction in Pancreatic Beta-Cells

All cellular processes are controlled by signals. Defects in the transduction of these signals cause disease. Although we have learned a great deal about the events that control a variety of functions in pancreatic beta-cells, the signalling defects that cause diabetes remain to be elucidated. A major interest in the laboratory is the role of intracellular calcium stores, including those sensitive to IP3, ryanodine and NAADP, in beta-cell survival and function. Intracellular calcium homeostasis is vital to the survival of all cell types. We are particularly interested in the mechanisms by which dysfunctional intracellular calcium signalling leads to programmed cell death. Intracellular calcium stores have been linked to diabetes in previous studies. There is also strong evidence that ER-stress, resulting from lowered ER calcium levels in the beta-cell, plays a significant role in both rare and common forms of diabetes. We are currently using advanced biochemical and molecular techniques, including FRET-based imaging for calcium signals, to further this research.

Lipotoxicity and Gene-Environment Interactions in Type 2 Diabetes

One of the causes of type 2 diabetes is an increase in pancreatic beta-cell death, leading to insufficient insulin. Unfortunately, we still do not understand which genes are required for beta cell survival in the presence of high fat, so we are unable to design effective treatments to stop beta-cell death. For decades, medical research has primarily used a ‘candidate’ gene approach to study known proteins, one at a time, for their role in specific disease states. With the emergence of new technology and systems biology, it is now possible to simultaneously examine virtually all genes or proteins in a cell. These unbiased approaches reveal novel findings that could not have been predicted based on prior knowledge. We have used unbiased proteomic analysis to reveal part of the mechanism by which fatty acids kill beta-cells via ER-stress. The objective of this research program is to continue our proteomics-guided efforts to understand how fatty acids kill beta cells. In particular, we will focus how fatty acids alter the beta-cell’s quality control system for proteins such insulin. We use advanced molecular biology and microscopy to determine how fatty acids lead to the degradation of key proteins in beta-cells. This study will improve our understanding of the underlying causes of diabetes as we search for ways to prevent, manage and cure this disease. This project is supported by a grant-in-aid from the Canadian Diabetes Association.

Technical Expertise

• Optical single cell recording techniques, including multiple wavelength dye and fluorescent protein imaging (e.g. Fura calcium imaging, GFP-tagging and localization).
• Forster resonance energy transfer imaging (FRET), frequency domain fluorescence lifetime imaging microscopy (FLIM; FLIM-FRET).
• Total internal reflectance fluorescence imaging microscopy (TIRF).
• Advanced data analysis, techniques for image quantification and manipulation.
• 3D imaging and cell volume analysis in cardiomyocytes.
• High-content, high-throughput imaging.
• Proteomics (fluorescent 2D-DIGE), genomic analysis
• Primary culture of endocrine cells for physiological measurements of hormone secretion, production, gene expression, radioimmunoassay and ELISA.
• Immunohistochemistry, cell proliferation, apoptosis.
• Morphological identification of live cells.
• Single cell microinjection.
• Basic molecular biology, including shRNAi, gene manipulation.
• Basic cellular biochemistry, DNA ladders, Western blot.
• In vivo and in vitro phenotype analysis of transgenic and mutant mice.

R e f e r e e d   P u b l i c a t i o n s
  1. Lim GE, Albrecht T, Piske M, Sarai K, Lee JTC, Ramshaw HS, Sinha S, Guthridge MA, Acker-Palmer A, Lopez AF, Clee SM, Nislow C, Johnson JD*. (2015) 14-3-3z coordinates visceral fat adipogenesis. Nature Communications 6:7671-7688. [IF 5].
  2. Templeman NM, Clee SM, Johnson JD*. (2015) Suppression of hyperinsulinaemia in growing female mice provides long-term protection against obesity.Diabetologia: 1-11. [IF 6.6].
  3. Yang YHC, Wills QF, Johnson JD*. (2015) 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 58: 1239-1249. [IF 6.6].
  4. Albrecht T, Zhao Y, Nguyen TH, Campbell RE, Johnson JD*. (2015) Fluorescent biosensors illuminate calcium levels within defined beta-cell endosome subpopulations. Cell Calcium 57: 263-274. [IF 4.3].
  5. Albu RF, Chan GT, Zhu M, Wong ETC, Taghizadeh F, Hu X, Mehran AE, Johnson JD, Gsponer J, Mayor T. (2015) A feature analysis of lower solubility proteins in three eukaryotic systems. Journal of Proteomics118:21-38. [IF 4.1].
  6. Chan MT, Lim GE, Skovsø S, Yang YHC, Albrecht T, Alejandro EU, Hoesli C, Piret JM, Warnock GL, Johnson JD*. (2014) Effects of insulin on human pancreatic cancer progression modeled in vitro. BMC Cancer 14: 814. [IF 3.3].
  7. Johnson JD*. (2014) A practical guide to genetic engineering of pancreatic beta-cells in vivo: Getting a grip on RIP and MIP. Islets 6: e944439. [IF 1.5].
  8. Liu Y, Wang R, Sun B, Mi T, Zhang J, Mu Y, Chen J, Bround MJ, Johnson JD, Gillis A, Chen SRW. (2014) Generation and characterization of a knock-in mouse model harboring the exon-3 deletion in the cardiac ryanodine receptor. PLoS One 9:e95615. [IF 3.8].
  9. Yang YHC, Vilin YY, Roberge M, Kurata HT, Johnson JD*. (2014) Multi-parameter screening reveals a role for Na+ channels in cytokine-induced beta-cell death. Molecular Endocrinology 28:406-17. [IF 4.7].
  10. Zhang D, Wan A, Chiu AP, Wang Y, Wang F, Neumaier K, Bround MJ, Johnson JD, Vlodavsky I, Rodrigues B. (2013) Hyperglycemia-induced secretion of endothelial heparanase stimulates a VEGF autocrine network in cardiomyocytes that promotes recruitment of LPL. Arteriosclerosis, Thrombosis, and Vascular Biology 33:2830-8. [IF 6.0].
  11. Szabat M, Johnson JD*. (2013) Modulation of b-cell fate and function by TGFb: A superfamily with many powers. Endocrinology 154: 3965. [IF 4.7].
  12. Yang YHC, Manning-Fox JE, Zhang KL, MacDonald PE, Johnson JD*. (2013) Intraislet SLIT-ROBO signaling is required for beta-cell survival and potentiates insulin secretion. PNAS 110:16480-5. [IF 9.7].
  13. Yang YHC, Johnson JD*. (2013) Multi-parameter, single-cell, kinetic imaging reveals multiple cell death modes in primary pancreatic beta-cells. Journal of Cell Science 126:4286-4295. [IF 6.1].
  14. Bround MJ, Wambolt R, Luciani DS, Kulpa JE, Rodrigues B, Brownsey RW, Moore EDW, Allard MF, Johnson JD*. (2013) Cardiomyocyte ATP production, metabolic flexibility, and survival require calcium flux through cardiac ryanodine receptors in vivo. J Biol Chem. 288: 18975-18986. [IF 4.5].
  15. Wang M, Li J, Lim GE, Johnson JD*. (2013) Is dynamic autocrine insulin signaling possible? A mathematical model predicts picomolar concentrations of extracellular monomeric insulin within human pancreatic islets. PloS one 8: e64860. [IF 4.3].
  16. Lim GE, Piske M, Johnson JD*. (2013) 14-3-3 proteins are essential signalling hubs for beta cell survival. Diabetologia 56: 825-837. [IF 6.8].
  17. Mehran AE, Templeman NM, Brigidi GS, Lim GE, Chu K-Y, Hu X, Botezelli JD, Asadi A, Hoffman BG, Kieffer TJ, Bamji SX, Clee SM, Johnson JD*. (2012) Hyperinsulinemia drives diet-induced obesity independently of brain insulin production. Cell Metabolism 16: 723–737. [IF 18].
  18. Bround MJ, Asghari P, Wambolt R, Bohunek L, Smits C, Philit M, Kieffer TJ, Lakatta EG, Boheler KR, Moore EDW, Allard MF, Johnson JD*. (2012) Cardiac ryanodine receptors control heart rate and rhythmicity in adult mice. Cardiovascular Research96:372-80. [IF 6.1].
  19. Luciani DS, White SA, Widenmaier S, Saran V, Taghizadeh F, Hu X, Allard MF, Johnson JD*. (2012). Bcl-2 and Bcl-xL suppress glucose signalling in pancreatic beta-cells. Diabetes 62:170-82. [IF 9.0].
  20. Hoesli C, Johnson JD, Piret JM. (2012). Purified Human Pancreatic Duct Cell Culture Conditions Defined by Serum-Free High-Content Growth Factor Screening. PLoS One 7:e33999. [IF 3.4].
  21. Szabat M, Lynn FC, Hoffman BG, Kieffer TJ, Allan DW, Johnson JD*. (2012) Maintenance of b-cell maturity and plasticity in the adult pancreas: Developmental biology concepts in adult physiology. Diabetes 61: 1365-1371. [IF 9.0].
  22. Kruit J, Wijesekara N, Westwell-Roper C, Vanmierlo T, de Haan W, Bhattacharjee A, Tang R, Wellington C, LutJohann D, Johnson JD, Brunham L, Verchere CB, Hayden MR. (2012). Loss of both ABCA1 and ABCG1 results in increased disturbances in islet sterol homeostasis, inflammation and impaired β-cell function. Diabetes 61:659-64. [IF 9.0].
  23. Wang F, Wang Y, Zhang D, Puthanveetil P, Johnson JD, Abrahani A, Rodrigues B. (2011). Fatty acid-induced nuclear translocation of heparanase uncouples glucose metabolism in endothelial cells. Arteriosclerosis, Thrombosis and Vascular Biology 32:406-14. [IF 7.2].
  24. Szabat M*, Kalynyak TB*, Lim GE, Chu KY, Yang YH, Asadi A, Gage BK, Ao Z, Warnock GL, Piret JM, Kieffer TJ, Johnson JD*. (2011). Musashi expression in β-cells coordinates insulin expression, apoptosis and proliferation in response to endoplasmic reticulum stress in diabetes. Cell Death and Disease 2:e232. [IF 5.3].
  25. Kruit JK, Wijesekara N, Manning Fox JE, Dai X-Q, Brunham LR, Searle GJ, Morgan GP, Costin AJ, Tang R, Johnson JD, Light PE, Marsh BJ, MacDonald PE, Verchere CB, Hayden MR. (2011). Islet cholesterol accumulation due to loss of ABCA1 leads to impaired exocytosis of insulin granules. Diabetes 60:3186-96. [IF 8.5].
  26. Chu KY, Li H, Wada K, Johnson JD*. (2011) Ubiquitin C-terminal hydrolase L1 is required for b-cell survival and function in lipotoxicity. Diabetologia 285:32606-15. [IF 6.6].
  27. Alejandro EU, Lim GE, Mehran AE, Hu X, Taghizadeh F, Pelipeychenko D, Baccarini M, Johnson JD*. (2011) Pancreatic beta-cell Raf-1 is required for glucose tolerance, insulin secretion and insulin 2 transcription. FASEB J 25:3884-95. [IF 6].
  28. Szabat M, Pourghaderi P, Soukhatcheva G, Verchere CB, Warnock GL, Piret JM, Johnson JD*. (2011). Kinetics and genomic profiling of adult human and mouse β-cell maturation. Islets 3: 175-87. [IF 1.5].
  29. Chu KY, Briggs MJL, Albrecht T, Drain PF, Johnson JD*. (2011). Differential regulation and localization of carboxypeptidase D and carboxypeptidase E in human and mouse β-cells. Islets 3: 155-165. [IF 1.5].
  30. Gallo M, Park D, Luciani DS, Kida K, Palmieri F, Blacque OE, Johnson JD, Riddle DL. (2011). MISC-1/OGC links mitochondrial metabolism, apoptosis and insulin secretion. PLoS One 6:e17827. [IF 4.3].
  31. Yang YHC, Szabat M, Bragagnini C, Kott K, Helgason CD, Hoffman BG, Johnson JD*. (2011) Paracrine signaling loops in adult pancreatic islets: Netrins modulate beta-cell apoptosis via Neogenin and Unc5a. Diabetologia 54:828-42. [IF 6.6]. /C14.
  32. Hoesli CA, Raghuram K, Kiang R, Mocinecová D, Hu X, Johnson JD, Lacík I, Kieffer TJ, Piret JM. (2010) Pancreatic Cell Immobilization in Alginate Beads Produced by Emulsion and Internal Gelation. Biotechnology & Bioengineering 108: 424-434. [IF 4.1].
  33. Hill JA, Szabat M, Hoesli CA, Gage BK, Yang YH, Williams DE, Riedel MJ, Luciani DS, Kalynyak TB, Tsai K, Ao Z, Andersen RJ, Warnock GL, Piret JM, Kieffer TJ, Johnson JD*. (2010) Multi-parameter, high-content, high-throughput screening for regulators of betacell fate and function. PLoS One 5:e12958. [IF 4]. /C7
  34. Chu KY, Lin Y, Hendel A, Kulpa JE, Brownsey RW, Johnson JD*. (2010) ATP-citrate lyase reduction mediates palmitate-induced apoptosis in pancreatic beta-cells. J Biol Chem. 285:32606-15. [IF 4.6]. /C38
  35. Bernal-Mizrachi E, Cras-Méneur C, Johnson JD, Permutt MA. (2010) Transgenic overexpression of active calcineurin in beta-cells results in decreased beta-cell mass and hyperglycemia in mice. PLos One 5:e11969. [IF 4.3].
  36. Szabat, M, Johnson, JD*, Piret JM. (2010) Reciprocal modulation of adult beta-cell maturity by activin A and follistatin. Diabetologia 53: 1680-9. [IF 6.4]. /C34
  37. Wang F, Wang Y, Kim M, Puthanveetil P, Ghosh S, Luciani DS, Johnson JD, Abrahani A, Rodrigues B. (2010) Glucose-induced endothelial heparanase secretion requires cortical and stress actin reorganization. Cardiovascular research 87: 127-136. [IF 5]. /C22
  38. Hutton MJH, Soukhatcheva G, Johnson JD, Verchere CB. (2010). Role of the TLR signaling molecule TRIF in beta-cell function and glucose homeostasis. Islets :104-11. [IF 1.5]. /13
  39. Alejandro EU, Kalynyak TB, Taghizadeh T, Gwiazda KS, Rawstrom EK, Jacob KJ, Johnson JD*. (2010). Acute insulin signaling in pancreatic beta-cells is mediated by multiple Raf-1 dependent pathways. Endocrinology 151:502-12. [IF 4]. /C31
  40. Fujimoto K, Hanson PT, Tran H, Ford EL, Han Z, Johnson JD, Levine B, Schimdt B, Wice BM, Polonsky KS. (2009). Autophagy regulates pancreatic beta cell death in response to Pdx1 deficiency and nutrient deprivation. J Biol Chem. 284:27664-73. [IF 8].
  41. Johnson JD*, Otani K, Bell GI, Polonsky KS. (2009).Impaired insulin secretion in transgenic mice over-expressing calpastatin in pancreatic β-cells. Islets 1:242-8. [IF 1]. /C4.
  42. Kewalramani G, Puthanveetil P, Wang F, Kim MS, Deppe S, Abrahani A, Luciani DS, Johnson JD, Rodrigues B. (2009). AMP-activated protein kinase confers protection against TNF-alpha induced cardiac cell death. Cardiovascular Research 84: 42-53. [IF 9].
  43. Li J, Johnson JD*. (2009). Mathematical models of subcutaneous injection of insulin analogues: A mini-review. Discrete Continuous Dyn Syst Ser B12:401-14. [IF 9].
  44. Johnson JD*, Ao Z, Ao P, Li H, Dai L, He Z, Tee M, Potter KJ, Meloche RM, Thompson DM, Verchere CB, Warnock GL. (2009) Different effects of FK506, rapamycin, and mycophenolate mofetil on glucose-stimulated insulin release and apoptosis in human islets. Cell Transplantation 18: 833-845. [IF 9].
  45. Gwiazda K, Yang TB, Lin Y, Johnson JD*. (2009). Effects of palmitate on ER and cytosolic Ca2+ homeostasis in b-cells. American Journal of Physiology 296: E690-E701. [IF 1].
Further publications can be found here.
L a b   M e m b e r s
Dr. James D. Johnson, Ph.D. (Group Leader)
Dr. Evgeniy Panzhinskiy, Ph.D. (Post-doctoral Fellow)
Dr. Søs Skovsø, Ph.D. (Post-doctoral Fellow)
Dr. Honey Modi, Ph.D. (Post-doctoral Fellow)
Dr. Jelena Kolic, Ph.D. (Post-doctoral Fellow)
Dr. Diego Bottezelli, Ph.D. (Visiting Post-doctoral Fellow)
Ms. Leanne Beet, B.Sc. (Staff & Lab Manager)
Ms. Betty Hu, M.Sc. (Staff)
Mr. Howard Cen, B.Sc. (Graduate Student)
Ms. Stephanie Marcil, B.Sc. (Post-graduate Student)
Ms. Anni Zhang, B.Sc. (Graduate Student)
Mr. Sepehr Kamal, B.Sc. (Graduate Student)
Ms. Jennifer Wildi (Undergraduate Student)
Mr. Jamie Magrill (Undergraduate Student)
J o i n   t h e   L a b

The Laboratory for Molecular Signalling in Diabetes is looking for exceptional students and post-doctoral fellows.

Potential applicants should be highly motivated. Potential students should have a strong interest in pursuing a career in research and be competitive for external scholarships. Post-doctoral applicants should have experience in a relevant research area, a strong publication record and be competitive for external fellowship awards.

Please contact Dr. Johnson directly by e-mail if you are interested. Include a curriculum vitae (with grades for students), a statement of career goals, and an outline of the specific research you see yourself doing in the lab.