个人简介

After completing his PhD in Medicine at the University of Liverpool, Dr Turner moved to the USA to undertake postdoctoral studies at The Scripps Research Institute, Harvard Medical School, and Albert Einstein College of Medicine. He then returned to the UK to take up a faculty appointment at Bart's and The London School of Medicine and Dentistry, before later moving to his current position here at Nottingham Trent University.

研究领域

diabetes, insulin secretion, TNFR-associated periodic syndrome (TRAPS)

Research in the Turner laboratory focuses upon identifying molecular causes of disease. Specific areas of research are as follows: Neuroendocrine Secretory Mechanisms Controlled release of hormones, neurotransmitters, and inflammatory cytokines from 'professional' secretory cells is essential in order for human survival, and occurs as a result of stimulated exocytotic fusion of secretory granules / vesicles with the cell surface plasma membrane. Projects typically investigate the cellular machinery regulating vesicular transport and granule fusion events, and the molecular mechanisms triggering disruption to these processes in type 2 diabetes and other diseases. Diet and Diabetes Elevated circulating glucose and fatty acid concentrations are known to trigger and exacerbate type 2 diabetes. We are interested in identifying molecules that potentially have a major impact in terms of pancreatic cell function and diabetogenesis. Recent work utilizing Affymetrix microarray analysis has identified clusters of genes whose expression level is modulated by glucolipotoxicity, and we have now uncovered a number of pathways and individual targets that form the basis for current and upcoming projects. In addition, we are also investigating the protective effects of vitamin D upon pancreatic cell survival and function. Immune Cell Signalling in Inflammatory Diseases Response to infection or autoinflammation is in part mediated by the cytokine, tumor necrosis factor (TNF), and the effects of TNF are in turn mediated by two receptors, TNFR1 and TNFR2. We are investigating the relationship between TNFR mutations and immune cell function in inflammatory diseases.

近期论文

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TNFR1 trafficking dysfunction opens the TRAPS door to proinflammatory cytokine secretion. Turner MD, Chaudhry,A, and Nedjai B, Biosci. Rep, 2012, 32, 105-112 Class II phosphoinositide 3-kinase regulates exocytosis of insulin granules in pancreatic beta cells. Dominguez V, Raimondi C, Somanath S, Bugliani M, Loder MK, Edling CE, Divecha N, da Silva-Xavier G, Marselli L, Persaud SJ, Turner M D, Rutter GA, Marchetti P, Falasca M, and Maffucci T J. Biol. Chem. 2011, 286, 4216-4225 Differential cytokine secretion resulting from p65 and c-Rel NF-kappaB subunit signaling in peripheral blood mononuclear cells of TNFR-associated periodic fever syndrome patients. Nedjai B, Hitman GA, Church LD, Minden K, Whiteford ML, McKee S, Stjernberg S, Pettersson T, Ranki A, Hawkins P, Arkwright PD, McDermott MF and Turner MD,Cell. Immunol. 2011, 268, 55-59 Lessons from anti-TNF biologics: infliximab failure in a TRAPS family with the T50M mutation in TNFRSF1A. Nedjai B, Quillinan N, Coughlan RJ, Church L, McDermott MF, Hitman GA, and Turner MD, Adv. Exp. Med. Biol, 2011, 691, 409-419 Comment on: Low TNF-induced NF-kappaB and p38 phosphorylation levels in leucocytes in tumour necrosis factor receptor-associated periodic syndrome. Turner MD and Chernajovsky Y. Rheumatology, 2011, 50, 1525-1526 Proinflammatory action of the antiinflammatory drug infliximab in TNF-receptor associated periodic syndrome. Nedjai B, Hitman GA, Quillinan N, Coughlan RJ, Church LD, McDermott MF and Turner MD, Arthritis Rheum, 2009, 60, 619-625 A novel TNFRSF1A splice mutation associated with increased nuclear factor kappa appaB (NF-kappa B) transcription factor activation in patients with tumour necrosis factor receptor associated periodic syndrome (TRAPS). Churchman SM, Church LD, SAvic S, Coulthard LR, Haywood B, Nedjai B, Mcdermot MF, Turner MD, Matthews RJ, Bagueley E, Hitman GA, Gooi HC, Wood P, Emery P Annals of the Rheumatic Diseases, 2008, 67 (11), 1589 Abnormal tumor necrosis factor receptor I cell surface expression and NF-kappa B activation in tumor necrosis factor receptor-associated periodic syndrome. Nedjai B, Hitman GA, Yousaf N, Chermajovsky Y, Stjernberg-Salmela S, Pettersson T, Ranki A, Hawkins PN, Arkwright PD, Mcdermott MF, Turner MD, Arthritis and Rheumatism, 2008, 58 (1), 273-283