Associate Professor Trevor Biden
Principal Research Fellow; Director, Diabetes Signalling Unit; Group Leader, Cell Signalling Group, Diabetes and Obesity Research Program, Garvan Institute of Medical Research; Associate Professor, Faculty of Medicine, The University of New South Wales
Email: t.biden 'at' garvan.org.au
Research Group: Biden
In ensuing years, Trevor's original group has developed into a Unit, but still continues to focus on the nexus between signalling, cellular function and the pathophysiology of diabetes, be it investigating the molecular mechanisms of insulin resistance, or pancreatic beta cell dysfunction. He believes that the team’s current projects - endoplasmic reticulum stress in beta cells, and the surprising re-emergence of PKC as a therapeutic target for diabetes, are some of the most exciting of his career. He feels fortunate to have been a part of the tremendous development of the Garvan over the last 15 years.
Education
1983 PhD University of London, London, UK
1979 BSc (Hons) University of Sydney
Awards and Honours
1989-92 Juvenile Diabetes Foundation International Career Development Award
1987-89 Queen Elizabeth II Australian National Research Fellowship
Publications
Schmitz-Peiffer C, Laybutt DR, Narasimhan S, Burchfield JG, Mitchell CJ, Gurisik E, Braun U, Cooney GJ, Leitges M and Biden TJ. Inhibition of PKCe improves glucose-stimulated insulin secretion and reduces insulin clearance. Cell Metab. 2007 6, 320-328.
Laybutt, DR, Preston AM, Akerfeldt MC, Busch AK, Biankin AV, and Biden, T.J. Endoplasmic Reticulum Stress Contributes to ≤-Cell Apoptosis in Type 2 Diabetes. Diabetologia 2007; 50, 752-763
Ludowyke RI, Elgundi Z, Kranenburg T, Stehn JR, Schmitz-Peiffer C, Hughes WE, Biden TJ. Phosphorylation of nonmuscle myosin heavy chain IIA on Ser1917 is mediated by protein kinase C beta II and coincides with the onset of stimulated degranulation of RBL-2H3 mast cells. J Immunol 2006; 177(3):1492-9.
Busch AK, Gurisik E, Cordery DV, Sudlow M, Denyer GS, Laybutt DR, Hughes WE, Biden TJ. Increased fatty acid desaturation and enhanced expression of stearoyl coenzyme A desaturase protects pancreatic beta-cells from lipoapoptosis. Diabetes 2005; 54(10):2917-24.
Busch AK, Cordery D, Denyer GS, Biden TJ. Expression-profiling of palmitate- and oleate-regulated genes provides novel insights into the effects of chronic lipid exposure on pancreatic β-cell function. Diabetes 2002; 51:977-987.
Carpenter L, Mitchell CJ, Xu ZZ, Poronik P, Both GW, Biden TJ. PKC alpha is activated but not required during glucose-induced insulin secretion from rat pancreatic islets. Diabetes 2004; 53(1):53-60.
Carpenter L, Cordery D, Biden TJ. Protein kinase C δ activation by interleukin-1β stabilizes inducible nitric-oxide synthase mRNA in pancreatic β-cells. J Biol Chem 2001; 276:5368-5374.
Schmitz-Peiffer C, Craig DL, Biden TJ. Ceramide generation is sufficient to account for the inhibition of insulin-stimulated PKB pathway in C2C12 skeletal muscle cells pretreated with palmitate. J Biol Chem 1999; 274:24202-24210.
Schmitz-Peiffer C, Browne CL, Watkinson A, Oakes ND, Chisholm DJ, Kraegen EW, Biden TJ. Alterations in the expression and cellular localization of protein kinase C isozymes θ and ε are associated with insulin resistance in skeletal muscle of the high-fat-fed rat. Diabetes 1997; 46:169-178.
Selbie LA, Schmitz-Peiffer C, Sheng Y, Biden TJ. Molecular cloning and characterization of PKCi, an atypical isoform of protein kinase C derived from insulin-secreting cells. J Biol Chem 1993; 268:24296-24302.
