An NCI-designated Comprehensive Cancer Center

The Thurmond Lab

Debbie Thurmond Islet Cell Research | City of Hope
The Thurmond Lab seeks to identify cellular and molecular mechanisms behind diabetes development and find therapies that can stop or reverse the disease’s progression.
Debbie Thurmond Islet Cell Research | City of Hope
Our science centers on multitaskers, messenger proteins that play a beneficial role across multiple types of tissue. In this case, those proteins both increase the production of insulin — essential to the body’s ability to process sugar — and improve the capacity of skeletal muscle to make use of insulin.
 
 
What we discover about how those proteins work and how to manipulate them ultimately will help to develop innovative cellular treatments for fighting type 1 and type 2 diabetes, in collaboration with our scientific and clinical colleagues at City of Hope. Other projects in the Thurmond Lab focus on how these multitaskers can improve islet cell transplantation—a promising investigational treatment for type 1 diabetes—and can serve as biomarkers for detecting the development of diabetes.
 
If you would like more information about the Thurmond lab, please contact us at 626-256-4673.

Principal Investigator

Debbie C. Thurmond, Ph.D.
Ruth B. & Robert K. Lanman Chair in Gene Regulation and Drug Discovery Research
Role: Principal Investigator
Research Focus: Molecular and Cellular Endocrinology
Cellular pathways/mechanisms of insulin release and blood glucose control
Cellular therapies to treat type-1 and type-2 diabetes
Improving islet cell transplantation
Biomarkers for detecting diabetes development

Principal Investigator

Debbie C. Thurmond, Ph.D.
Ruth B. & Robert K. Lanman Chair in Gene Regulation and Drug Discovery Research
Role:Principal Investigator
Research Focus: Molecular and Cellular Endocrinology; Cellular pathways/mechanisms of insulin release and blood glucose control; Cellular therapies to treat type-1 and type-2 diabetes; Improving islet cell transplantation; Biomarkers for detecting diabetes development

Lab Members

Eunjin Oh, Ph.D.
Assistant Research Professor
 
Raja Veluthakal, Ph.D.
Assistant Research Professor
 
Miwon Ahn, Ph.D.
Staff Scientist
 
Karla E. Merz
Predoctoral Graduate Student
 
Erika Olsen
Research Associate
 
Mariann Chang
Research Associate

Lab Publications

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Restoration of Glucose-Stimulated Cdc42-Pak1 Activation and Insulin Secretion by a Selective Epac Activator in Type 2 Diabetic Human Islets.
Veluthakal R, Chepurny OG, Leech CA, Schwede F, Holz GG, Thurmond DC. Diabetes. 2018 Jul 9. [Epub ahead of print]
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Novel approaches to restore beta cell function in prediabetes and type 2 diabetes.
Salunkhe VA, Veluthakal R, Kahn SE, Thurmond DC. Diabetologia. 2018 Sep;61(9):1895-1901. Epub 2018 Jun 8.
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Doc2b Protects β-Cells Against Inflammatory Damage and Enhances Function.
Aslamy A, Oh E, Olson EM, Zhang J, Ahn M, Moin ASM, Tunduguru R, Salunkhe VA, Veluthakal R, Thurmond DC. Diabetes. 2018 Jul;67(7):1332-1344. Epub 2018 Apr 16
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Exocytosis Protein DOC2B as a Biomarker of Type 1 Diabetes.
Aslamy A, Oh E, Ahn M, Moin ASM, Chang M, Duncan M, Hacker-Stratton J, El-Shahawy M, Kandeel F, DiMeglio LA, Thurmond DC. J Clin Endocrinol Metab. 2018 May 1;103(5):1966-1976.
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Depletion of the membrane-fusion regulator Munc18c attenuates caerulein hyperstimulation-induced pancreatitis.
Dolai S, Liang T, Orabi AI, Xie L, Holmyard D, Javed TA, Fernandez NA, Xie H, Cattral MS, Thurmond DC, Thorn P, Gaisano HY. J Biol Chem. 2018 Feb 16;293(7):2510-2522. Epub 2017 Dec 28.

THURMOND LAB RESEARCH HIGHLIGHTS

The Thurmond Lab’s focus encompasses research into SNARE-mediated vesicle trafficking events and cytoskeletal signaling as they pertain to the causes of diabetes. We have discovered that people with diabetes harbor defects and deficiencies in certain vesicle trafficking proteins. We are actively devising strategies to remediate these defects.
 
The proteins that we study — syntaxin 4 (STX4), p21-activated kinase (PAK1) and Doc2b — play significant roles in insulin production, as well as insulin and glucose uptake by skeletal muscle and fat tissues. We have found that depleted STX4 and PAK1 reduce insulin release and sensitivity, while overexpression of STX4 and Doc2b lead to improved glucose control. We are exploring therapeutic approaches that can restore or raise STX4 and Doc2b levels to increase insulin secretion and overcome insulin resistance among diabetes patients and those at risk of developing type 1 or type 2 diabetes.
 
Another goal is to make islet cell transplantation available to more patients. We are zeroing in on STX4 — which has the ability to activate dormant insulin-producing beta cells — to determine whether we can take advantage of the protein’s action to modify the islet cell transplant so that it uses fewer cells. Success in this endeavor would make possible more transplants from the limited resource of cells donated by humans.
 
The Thurmond Lab also is examining STX4 and PAK1 as potential biomarkers for diabetes. If these proteins can help us to detect early diabetic changes, patients can receive more timely interventions that preserve islet cell function and improve blood glucose control. A related project meant to expand our understanding of diabetes is exploring how production and use of STX4 and PAK1 are influenced by risk factors such as obesity, inflammation or a diet high in fat and sugar.