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Natasha J. Hill

Researcher at Kingston University

Publications -  28
Citations -  1367

Natasha J. Hill is an academic researcher from Kingston University. The author has contributed to research in topics: Congenic & NOD mice. The author has an hindex of 15, co-authored 28 publications receiving 1313 citations. Previous affiliations of Natasha J. Hill include Scripps Research Institute & University of Cambridge.

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The NOD Idd9 Genetic Interval Influences the Pathogenicity of Insulitis and Contains Molecular Variants of Cd30, Tnfr2, and Cd137

TL;DR: Evidence for the existence of a gene only influencing diabetes, Idd9 on mouse chromosome 4, is provided by the development of a novel congenic mouse strain, NOD, which displays profound resistance to diabetes even though nearly all develop insulitis.
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NOD Idd5 locus controls insulitis and diabetes and overlaps the orthologous CTLA4/IDDM12 and NRAMP1 loci in humans.

TL;DR: The Idd5 locus provides a significant amount of protection from diabetes (50% reduction from parental frequency) and when combined with another resistance locus (Idd3 on chromosome 3), provides nearly completeprotection from diabetes and insulitis.
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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.

TL;DR: All of the current data support the hypothesis that Idd3 corresponds to amino acid variation at the amino terminus of Il2, and suggest that the profound protection from diabetes seen in congenic mice carrying an I dd3 protective allele is unlikely to be due to differences in the level of expression of the Il2 gene.
Journal Article

Congenic mapping of the insulin-dependent diabetes (Idd) gene, Idd10, localizes two genes mediating the Idd10 effect and eliminates the candidate Fcgr1.

TL;DR: The study on chromosome 3 begins to reveal the extent of the polygenic nature of autoimmune diabetes, and demonstrates that the use of congenic strains is an effective mapping strategy, even in the dissection of multiple, linked genes with subtle effects.
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Mapping of the IDDM locus Idd3 to a 0.35-cM interval containing the interleukin-2 gene.

TL;DR: Congenic mapping of the Idd3 locus provided circumstantial evidence in support of the hypothesis that Idd2 is an allelic variation of the Il2 gene, or a variant in strong linkage disequilibrium.