Dr Natasha Hill
School/Department: Life Sciences, Pharmacy & Chemistry
Position: Senior Lecturer in Genetics and Molecular Biology
I graduated from Bristol University with a degree in Biochemistry and went on to study for a PhD in the Genetics of Type 1 diabetes at Oxford, under the supervision of Prof John Todd. I then moved to the USA to work with Dr Nora Sarvetnick at The Scripps Research Institute in La Jolla, focusing on the development of autoimmunity and regulation by a particular gene variant in the non-obese diabetic (NOD) model of type 1 diabetes. I returned to the UK and worked briefly as an independent research fellow at the Blizard Institute in Whitechapel, part of Barts and The London Queen Mary School of Medicine and Dentistry, before obtaining a permanent position at Kingston University in 2008. My research interests are now focused on finding novel approaches to promote islet regeneration, and my lab also has an interest in pancreatic cancer. I currently teach genetics and molecular biology at an undergraduate level as well as contributing to teaching on the Cancer Biology and Biotechnology MSc degrees.
Educational and Professional Qualifications
- 1995 - 1999 DPhil 'Genetics of Type 1 Diabetes' at Oxford University
- 1991 - 1994 BSc Hons in Biochemistry at Bristol University
Diabetes, islet regeneration, autoimmunity, pancreatic cancer
Diabetes Research Group website
Genetics and molecular biology
Other Professional Activity
In 2012 I set up the Diabetes and Cardiovascular Research Group to promote interdisciplinary research in this area at Kingston, which now forms part of the IhSHA research hub. I am also a member of the Society of Biology. My own research group consists of PhD and MScR students, and I also supervise MSc summer projects and undergraduate internships. I have reviewed grants for various funding agencies, including Diabetes UK, the MRC and the BBSRC, and well as manuscripts for a range of immunology and cell biology journals.
Viloria K and Hill NJ. Embracing the complexity of matricellular proteins: the functional and clinical significance of splice variation. Biomol Concepts. 2016 May 1;7(2):117-132.
Ryall CL, Viloria K, Lhaf F, Walker AJ, King A, Jones P, Mackintosh D, McNeice R, Kocher H, Flodstrom-Tullberg M, Edling C, Hill NJ. Novel role for matricellular proteins in the regulation of islet β cell survival: the effect of SPARC on survival, proliferation and signalling. J Biol Chem. 2014 Sep 9. pii: jbc.M114.573980.
McGuire HM, Vogelzang A, Hill N, Flodström-Tullberg M, Sprent J, King C. Loss of parity between IL-2 and IL-21 in the NOD Idd3 locus. Proc Natl Acad Sci U S A. 2009 Nov 17;106(46):19438-43. Epub 2009 Oct 30.
Yadav, D, Hill NJ, Yagita H, Azuma M, Sarvetnick N. Altered availability of PD-1/PD ligands is associated with the failure to control autoimmunity in NOD mice, Cell. Immunol. 2009, 258(2):161-71. Epub 2009 May 6.
Hill NJ, King C, Flodstrom-Tullberg M. Recent acquisitions on the genetic basis of autoimmune disease. Front Biosci. 2008 May 1;13:4838-51.
Hultcrantz M, Jacobson S, Hill NJ, Santamaria P, and Flodström-Tullberg M. The Target Cell Response to Cytokines Governs the Autoreactive T-cell Repertoire in the Pancreas. Diabetologia. 2009 Feb 52(2):299-305.
Hill NJ, Stotland A, Solomon M, Secrest P, Getzoff E, and Sarvetnick N. Resistance of the target islet tissue to autoimmune destruction contributes to genetic susceptibility in Type 1 diabetes. Biol Direct. 2007 Jan 25;2(1):5
Hill NJ, Hultcrantz M, Sarvetnick N, Flodström-Tullberg M. The target tissue in autoimmunity - an unforeseen niche with regulatory activity. Eur J Immunol. 2007 Mar; 37(3):587-97.
Hill NJ, Stotland A and Sarvetnick N. Distinct regulation of autoreactive CD4 T cells by IL4 under conditions of lymphopenia. J Leukoc Biol. 2007 Mar; 81(3):757-65.
Hill NJ, Van Gunst K and Sarvetnick N. Th1 and Th2 pancreatic inflammation differentially affect homing of islet-reactive CD4 T cells in the non-obese diabetic (NOD) mouse. J Immunol 2003 Feb;170(4):1649-58.
Hill NJ and Sarvetnick N. Cytokines: promoters and dampeners of autoimmunity. Curr Opinion Immunol 2002 Dec;14(6):791-7.
Hill NJ, PA Lyons, N Armitage, JA Todd, LS Wicker, LB Peterson. The NOD Idd5 locus controls insulitis and diabetes and overlaps the orthologous CTLA4/IDDM12 and NRAMP1 loci in humans. Diabetes 2000 Oct;49(10):(R)4-7.
Cordell HJ, Todd JA, Hill NJ, Lord CJ, Lyons PA, Peterson LB, Wicker LS, Clayton DG. Statistical modelling of inter-locus interactions in a complex disease: rejection of the multiplicative model of epistasis in type 1 diabetes. Genetics 2001 May;158(1):357-67.
Lyons PA, WW Hancock, P Denny, CJ Lord, NJ Hill, N Armitage, T Siegmund, JA Todd, MS Phillips, JF Hess, S-L Chen, PA. Fischer, LB Peterson, LS Wicker. The NOD Idd9 genetic interval influences the pathogenicity of insulitis and contains molecular variants of Cd30, Tnfr2, and Cd137. Immunity 2000 Jul;13(1):107-15.
Lyons PA, Armitage N, Argentina F, Denny P, Hill NJ, Lord CJ, Wilusz MB, Peterson LB, Wicker LS, Todd JA. Congenic mapping of the type 1 diabetes locus, Idd3, to a 780-kb region of mouse chromosome 3: identification of a candidate segment of ancestral DNA by haplotype mapping. Genome Res 2000 Apr;10(4):446-53.
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