Paul Squires

ORCID iD
https://orcid.org/0000-0003-4547-6777
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Professor Paul E. Squires

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Paul Squires (2016-03-06)

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United Kingdom

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Scopus to ORCID (2016-01-24)

  • Keywords
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Diabetes Research

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Paul Squires (2015-08-19)

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Website

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Paul Squires (2016-03-06)

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Scopus Author ID: 7004493480

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Scopus to ORCID (2016-03-06)

Biography

Professor in Biomedical Science (Diabetes & Endocrinology) My research into diabetes mellitus, aims to better understand the sub-cellular mechanisms that regulate insulin secretion and action in health and disease. A common theme linking our work is determining how cell-cell adhesion, cell-coupling and cell-to-cell communication synchronise cellular activity and function within the renal nephron and pancreatic islet. After studying for a PhD in GI motility, I remained at the University of Sheffield to work as a PDRA with Professor Mark Dunne (1992-95). During this period I helped identify that non-functional K+ATP-channels in pancreatic beta-cells, contributed to persistent hyperinsulinaemia, hypoglycaemia of infancy (Nature Med. 2, 1344-1347, 1996; Archiv.Child.Dis. 74, 373-378, 1996). These studies have implications for the pre-operative treatment of new-borns presenting with nesidioblastosis. In 1995 I was awarded a Royal Society Travelling Research Fellowship to work at the University of British Columbia with Prof Alison Buchan studying stimulus-response coupling in gastrin-secreting cells. My experience using live imaging of Ca2+-dynamics helped identify a novel role for the newly cloned calcium-sensing receptor (CaSR) in regulating endocrine secretory function (J. Clin. Invest. 99, 2328-2333, 1997; Gastroenterology. 112, 357-363, 1997; Gastroenterology. 120, 1128-1139, 2001). In 1998, I returned to the UK to join Prof Peter Jones and Shanta Persuad as a Diabetes UK funded RD Lawrence Research Fellow at KCL. The Diabetes Research Group were developing a model pseudo-islet system for improved insulin release (Diabetes. 48:1402-1408, 1999) and we demonstrated that the CaSR contributed to cell-to-cell coupling and communication within the islet (Diabetes 49. 409-417, 2000). The success of the work led to a ‘Paul Langerhans Award for research into the physiology and pathophysiology of the beta-cell from the EASD (Diabetologia. 44: (News) 45-46, 2001) and an Honorary Lectureship at KCL (2001-2004). Establishing an independent diabetes group at the University of Warwick in 2001, I became Reader in Diabetes & Endocrinology and took on the role of Course Director for Biomedical Science. In collaboration with Dr Claire Hills, my research interests diversified to include the study of renal complications of diabetes. This adjunct line of investigation has exposed a novel role for the pro-fibrotic cytokine TGFβ1 in glucose-evoked changes in cell-to-cell coupling and epithelial integrity (Am J Physiol (Renal), 291, F1045-F1051, 2006; Cell Physiol Biochem 24, 177-186, 2009 and Diabetologia, 55, 812-824, 2012; Diabetologia, 58, 233-241, 2015). Our research, collaborating with Dr Isaac Liu (nanotechnologist), suggests that glucose-evoked renal fibrosis is linked to changes in membrane dynamics and cell coupling. The work highlights the importance of cytoskeletal changes and membrane deformation in regulating cell-cell adhesion and communication (FEBS Letts, 588 1178-1183, 2014; Cellular & Molecular Bioengineering, 8 (1), 22-31, 2015). As part of a £14M expansion in Life Sciences, I moved to the University of Lincoln in September 2014, where diabetes is now a central research theme of the new Lincoln Institute for Health. I have published in excess of 70 research articles and had the pleasure of contributing to the Research Advisory Boards of Diabetes UK (2005-2012), the Diabetes Research & Wellness Foundation (DRWF: 2010-present), and the European Foundation for the Study of Diabetes (EFSD: 2012-present).
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