Hill, Natasha - Kingston University - School of Life Sciences

个人简介

1995 - 1999 DPhil 'Genetics of Type 1 Diabetes' at Oxford University 1991 - 1994 BSc Hons in Biochemistry at Bristol University

研究领域

Diabetes, islet regeneration, autoimmunity, pancreatic cancer

近期论文

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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, Flodstr?m-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 Flodstr?m-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, Flodstr?m-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.