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rdf:type |
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lifeskim:mentions |
umls-concept:C0017741,
umls-concept:C0033684,
umls-concept:C0041485,
umls-concept:C0332453,
umls-concept:C0567416,
umls-concept:C0599894,
umls-concept:C1256369,
umls-concept:C1274040,
umls-concept:C1419119,
umls-concept:C1515926,
umls-concept:C1521840
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pubmed:issue |
6
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pubmed:dateCreated |
2002-5-28
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pubmed:abstractText |
IA-2 is a major autoantigen in type 1 diabetes. Autoantibodies to IA-2 appear years before the development of clinical disease and are being widely used as predictive markers to identify individuals at risk for developing type 1 diabetes. IA-2 is an enzymatically inactive member of the transmembrane protein tyrosine phosphatase family and is an integral component of secretory granules in neuroendocrine cells. To study its function, we generated IA-2-deficient mice. Northern and Western blot analysis showed that neither IA-2 mRNA nor protein was expressed. Physical examination of the IA-2(- /-) animals and histological examination of tissues failed to reveal any abnormalities. Nonfasting blood glucose levels, measured over 6 months, were slightly elevated in male IA-2(-/-) as compared to IA-2(+ /+) littermates, but remained within the nondiabetic range. Glucose tolerance tests, however, revealed statistically significant elevation of glucose in both male and female IA-2(-/-) mice and depressed insulin release. In vitro glucose stimulation of isolated islets showed that male and female mice carrying the disrupted gene released 48% (P < 0.001) and 42% (P < 0.01) less insulin, respectively, than mice carrying the wild-type gene. We concluded that IA-2 is involved in glucose-stimulated insulin secretion.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0012-1797
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
51
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1842-50
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:12031972-Animals,
pubmed-meshheading:12031972-Autoantigens,
pubmed-meshheading:12031972-Blood Glucose,
pubmed-meshheading:12031972-Blotting, Northern,
pubmed-meshheading:12031972-Blotting, Western,
pubmed-meshheading:12031972-DNA Restriction Enzymes,
pubmed-meshheading:12031972-Female,
pubmed-meshheading:12031972-Gene Targeting,
pubmed-meshheading:12031972-Genetic Vectors,
pubmed-meshheading:12031972-Glucose Tolerance Test,
pubmed-meshheading:12031972-Immunohistochemistry,
pubmed-meshheading:12031972-Insulin,
pubmed-meshheading:12031972-Litter Size,
pubmed-meshheading:12031972-Male,
pubmed-meshheading:12031972-Membrane Proteins,
pubmed-meshheading:12031972-Mice,
pubmed-meshheading:12031972-Protein Tyrosine Phosphatase, Non-Receptor Type 1,
pubmed-meshheading:12031972-Protein Tyrosine Phosphatases,
pubmed-meshheading:12031972-Receptor-Like Protein Tyrosine Phosphatases, Class 8,
pubmed-meshheading:12031972-Transfection
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pubmed:year |
2002
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pubmed:articleTitle |
Targeted disruption of the protein tyrosine phosphatase-like molecule IA-2 results in alterations in glucose tolerance tests and insulin secretion.
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pubmed:affiliation |
Experimental Medicine Section, Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland, USA.
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pubmed:publicationType |
Journal Article
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