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dc.contributor.authorMordes, John P.
dc.contributor.authorLeif, Jean H.
dc.contributor.authorNovak, Stephen
dc.contributor.authorDeScipio, Cheryl
dc.contributor.authorGreiner, Dale L.
dc.contributor.authorBlankenhorn, Elizabeth P.
dc.date2022-08-11T08:10:01.000
dc.date.accessioned2022-08-23T16:52:18Z
dc.date.available2022-08-23T16:52:18Z
dc.date.issued2002-10-29
dc.date.submitted2008-07-09
dc.identifier.citation<p>Diabetes. 2002 Nov;51(11):3254-62.</p>
dc.identifier.issn0012-1797 (Print)
dc.identifier.pmid12401717
dc.identifier.urihttp://hdl.handle.net/20.500.14038/42027
dc.description.abstractViral antibody-free BBDR and WF rats never develop spontaneous diabetes. BBDR rats, however, develop autoimmune diabetes after perturbation of the immune system, e.g., by viral infection. We previously identified a disease-susceptibility locus in the BBDR rat, iddm4, which is associated with the development of autoimmune diabetes after treatment with polyinosinic:polycytidylic acid and an antibody that depletes ART2(+) regulatory cells. We have now developed lines of congenic WF.iddm4 rats and report that in an intercross of N5 generation WF.iddm4 rats, approximately 70% of animals either homozygous or heterozygous for the BBDR origin allele of iddm4 became hyperglycemic after treatment to induce diabetes. Fewer than 20% of rats expressing the WF origin allele of iddm4 became diabetic. Testing the progeny of various recombinant N5 WF.iddm4 congenic rats for susceptibility to diabetes suggests that iddm4 is centered on a small segment of chromosome 4 bounded by the proximal marker D4Rat135 and the distal marker D4Got51, an interval of
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=12401717&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4034451/
dc.subjectAdoptive Transfer
dc.subjectAlleles
dc.subjectAnimals
dc.subject*Chromosome Mapping
dc.subjectDiabetes Mellitus, Type 1
dc.subjectDisease Models, Animal
dc.subjectGenetic Markers
dc.subjectGenetic Predisposition to Disease
dc.subjectHomozygote
dc.subjectIslets of Langerhans
dc.subjectPancreatic Diseases
dc.subjectRats
dc.subjectRats, Mutant Strains
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleThe iddm4 locus segregates with diabetes susceptibility in congenic WF.iddm4 rats
dc.typeJournal Article
dc.source.journaltitleDiabetes
dc.source.volume51
dc.source.issue11
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/483
dc.identifier.contextkey544965
html.description.abstract<p>Viral antibody-free BBDR and WF rats never develop spontaneous diabetes. BBDR rats, however, develop autoimmune diabetes after perturbation of the immune system, e.g., by viral infection. We previously identified a disease-susceptibility locus in the BBDR rat, iddm4, which is associated with the development of autoimmune diabetes after treatment with polyinosinic:polycytidylic acid and an antibody that depletes ART2(+) regulatory cells. We have now developed lines of congenic WF.iddm4 rats and report that in an intercross of N5 generation WF.iddm4 rats, approximately 70% of animals either homozygous or heterozygous for the BBDR origin allele of iddm4 became hyperglycemic after treatment to induce diabetes. Fewer than 20% of rats expressing the WF origin allele of iddm4 became diabetic. Testing the progeny of various recombinant N5 WF.iddm4 congenic rats for susceptibility to diabetes suggests that iddm4 is centered on a small segment of chromosome 4 bounded by the proximal marker D4Rat135 and the distal marker D4Got51, an interval of</p>
dc.identifier.submissionpathoapubs/483
dc.contributor.departmentDepartment of Pathology
dc.contributor.departmentDepartment of Medicine, Diabetes Division
dc.source.pages3254-62


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