| pubmed-article:18718526 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18718526 | lifeskim:mentions | umls-concept:C0011847 | lld:lifeskim |
| pubmed-article:18718526 | lifeskim:mentions | umls-concept:C0443146 | lld:lifeskim |
| pubmed-article:18718526 | lifeskim:mentions | umls-concept:C0314603 | lld:lifeskim |
| pubmed-article:18718526 | lifeskim:mentions | umls-concept:C1996904 | lld:lifeskim |
| pubmed-article:18718526 | lifeskim:mentions | umls-concept:C0683598 | lld:lifeskim |
| pubmed-article:18718526 | lifeskim:mentions | umls-concept:C0205359 | lld:lifeskim |
| pubmed-article:18718526 | lifeskim:mentions | umls-concept:C1880497 | lld:lifeskim |
| pubmed-article:18718526 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:18718526 | pubmed:dateCreated | 2008-10-22 | lld:pubmed |
| pubmed-article:18718526 | pubmed:abstractText | ALR/Lt, a NOD-related mouse strain, was selected for resistance to alloxan free radical-mediated diabetes (ALD). Despite extensive genomic identity with NOD (>70%), ALR mice display strong resistance to autoimmune type 1 diabetes (T1D) due to both an unusual elevation in systemic antioxidant defenses and a reduction in cellular ROS production that extends to the beta cell level. Reciprocal backcross to NOD previously linked the ALR-derived T1D resistance to Chr. 3, 8, and 17 as well as to the ALR mt-Nd2(a) allele encoded by the mitochondrial genome (mtDNA). To determine whether any of the ALR-derived loci protecting against T1D also protected against ALD, 296 six-week-old F2 mice from reciprocal outcrosses were alloxan-treated and assessed for diabetes onset, and a genome-wide scan (GWS) was conducted. GWS linked mt-Nd2 as well as three nuclear loci with alloxan-induced diabetes. A dominant ALR-derived ALD resistance locus on Chr. 8 colocalized with the ALR-derived T1D resistance locus identified in the previous backcross analysis. In contrast, whereas ALR contributed a novel T1D resistance locus on Chr. 3 marked by Susp, a more proximal ALR-derived region marked by Il-2 contributed ALD susceptibility, not resistance. In addition, a locus was mapped on Chr. 2, where heterozygosity provided heightened susceptibility. Tests for alloxan sensitivity in ALR conplastic mice encoding the NOD mt-Nd2(c) allele and NOD mice congenic for the protective Chr. 8 locus supported our mapping results. Alloxan sensitivity was increased in ALR.mt(NOD) mice, whereas it was decreased by congenic introduction of ALR genome on Chr. 8 into NOD. These data demonstrate both similarities and differences in the genetic control of T1D versus ROS-induced diabetes. | lld:pubmed |
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| pubmed-article:18718526 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18718526 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18718526 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:18718526 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:18718526 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18718526 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:18718526 | pubmed:issn | 0891-5849 | lld:pubmed |
| pubmed-article:18718526 | pubmed:author | pubmed-author:ChenJingJ | lld:pubmed |
| pubmed-article:18718526 | pubmed:author | pubmed-author:LuYingY | lld:pubmed |
| pubmed-article:18718526 | pubmed:author | pubmed-author:LiRenhuaR | lld:pubmed |
| pubmed-article:18718526 | pubmed:author | pubmed-author:LeeChul-HoCH | lld:pubmed |
| pubmed-article:18718526 | pubmed:author | pubmed-author:LeiterEdward... | lld:pubmed |
| pubmed-article:18718526 | pubmed:author | pubmed-author:MathewsClayto... | lld:pubmed |
| pubmed-article:18718526 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:18718526 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:18718526 | pubmed:volume | 45 | lld:pubmed |
| pubmed-article:18718526 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18718526 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18718526 | pubmed:pagination | 1263-70 | lld:pubmed |
