Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
|
| pubmed:dateCreated |
1989-7-10
|
| pubmed:abstractText |
It has been suggested that one of the recessive genes controlling diabetes in non-obese diabetic mice is linked to the major histocompatibility complex. We, therefore, performed restriction fragment length polymorphism studies of major histocompatibility complex genes (class I, II, and III) in non-obese diabetic mice in comparison with those of their non-diabetic sister strains, non-obese non-diabetic, cataract, and ILI mice which were derived from the same Jcl-ICR mice as the non-obese diabetic mouse was. When class II and III probes and a minimum of four restriction enzymes were used, class II and III genes of non-obese diabetic mice were indistinguishable from those of cataract and ILI mice but totally different from those of non-obese non-diabetic mice. The studies also indicated that A beta, E beta, and C4-Slp genes of non-obese diabetic, cataract, and ILI mice, and A alpha, A beta, E beta and C4-Slp genes of non-obese non-diabetic mice are different from those of BALB/c and C57BL/6 mice, respectively. While non-obese non-diabetic mice expressed the E alpha gene, non-obese diabetic, cataract, and ILI mice appeared to carry a deletion in the 5' end of the E alpha gene resulting in failure to transcribe the E alpha gene. When class I probe was used, cataract mice showed very different band patterns from those of the other ICR-derived mice. It is suggested that non-obese diabetic, non-obese non-diabetic, and ILI mice contain only a single class I D region gene.(ABSTRACT TRUNCATED AT 250 WORDS)
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Feb
|
| pubmed:issn |
0012-186X
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
32
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
118-25
|
| pubmed:dateRevised |
2006-11-15
|
| pubmed:meshHeading |
pubmed-meshheading:2566547-Animals,
pubmed-meshheading:2566547-Blotting, Northern,
pubmed-meshheading:2566547-Blotting, Southern,
pubmed-meshheading:2566547-Chromosome Mapping,
pubmed-meshheading:2566547-Diabetes Mellitus, Experimental,
pubmed-meshheading:2566547-Genes, MHC Class I,
pubmed-meshheading:2566547-Genes, MHC Class II,
pubmed-meshheading:2566547-Major Histocompatibility Complex,
pubmed-meshheading:2566547-Mice,
pubmed-meshheading:2566547-Mice, Inbred BALB C,
pubmed-meshheading:2566547-Mice, Inbred C57BL,
pubmed-meshheading:2566547-Mice, Inbred ICR,
pubmed-meshheading:2566547-Mice, Inbred Strains,
pubmed-meshheading:2566547-Mice, Mutant Strains,
pubmed-meshheading:2566547-Polymorphism, Genetic,
pubmed-meshheading:2566547-Polymorphism, Restriction Fragment Length,
pubmed-meshheading:2566547-Species Specificity
|
| pubmed:year |
1989
|
| pubmed:articleTitle |
Restriction fragment length polymorphism analysis of major histocompatibility complex genes in the non-obese diabetic mouse strain and its non-diabetic sister strains.
|
| pubmed:affiliation |
Department of Microbiology and Immunology, Hamamatsu University School of Medicine, Japan.
|
| pubmed:publicationType |
Journal Article,
Comparative Study
|