ArticleThe Journal of clinical investigation1993
Detection of pancreatic islet 64,000 M(r) autoantigens in insulin-dependent diabetes distinct from glutamate decarboxylase.
Article in The Journal of clinical investigation, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 79 citations in OpenAlex.
- Expression, characterization, processing and immunogenicity of an insulin-dependent diabetes mellitus autoantigen, IA-2, in Sf-9 cells.Clinical and experimental immunology · 1998Article
- Cross reactivity between IA-2 and phogrin/IA-2beta in binding of autoantibodies in IDDM.Diabetologia · 1997Article
- An islet-cell protein tyrosine phosphatase is a likely precursor to the 37-kDa autoantigen in type 1 diabetes: human and macaque sequences, tissue distribution, unique and shared epitopes, and predictive autoantibodies.Molecular medicine (Cambridge, Mass.) · 1997Article
- Identification of a second transmembrane protein tyrosine phosphatase, IA-2beta, as an autoantigen in insulin-dependent diabetes mellitus: precursor of the 37-kDa tryptic fragment.Proceedings of the National Academy of Sciences of the United States of America · 1996Article
- Imogen 38: a novel 38-kD islet mitochondrial autoantigen recognized by T cells from a newly diagnosed type 1 diabetic patient.The Journal of clinical investigation · 1996Article
- The 37/40-kilodalton autoantigen in insulin-dependent diabetes mellitus is the putative tyrosine phosphatase IA-2.Proceedings of the National Academy of Sciences of the United States of America · 1995Article
- Relationship of the 37,000- and 40,000-M(r) tryptic fragments of islet antigens in insulin-dependent diabetes to the protein tyrosine phosphatase-like molecule IA-2 (ICA512).The Journal of clinical investigation · 1995Article
- Brain-reactive autoantibodies in BB/d rats do not recognize glutamic acid decarboxylase.Clinical and experimental immunology · 1995Article
- Molecular biology of IDDM.Diabetologia · 1994Article
- Slow metabolic deterioration towards diabetes in islet cell antibody positive patients with autoimmune polyendocrine disease.Diabetologia · 1994Article
- Autoantibodies in insulin-dependent diabetes mellitus.Journal of endocrinological investigationReview
- Prediction and prevention of type I diabetes.Journal of endocrinological investigationReview
- Autoantigens in type 1 diabetes mellitus.Journal of endocrinological investigationReview
- T-cell reactivity to 38 kD insulin-secretory granule protein in patients with recent onset type 1 diabetes.Journal of endocrinological investigationArticle
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Patients with insulin-dependent diabetes (IDDM) possess antibodies to islet proteins of M(r)-64,000. Potential autoantigens of this M(r) include glutamate decarboxylase (GAD) and 65 kD heat shock protein. We have detected two distinct antibody specificities in IDDM that bind 50,000 M(r) or 37,000/40,000 M(r) proteolytic fragments of 64,000 M(r) proteins. In this study, we investigated relationships of these proteolytic fragments to GAD and heat shock proteins. Polyclonal antibodies to GAD bound 50,000 M(r) fragments of islet antigen. Recombinant GAD65, but not GAD67, blocked binding to this antigen, suggesting that 50,000 M(r) fragments are derived from islet GAD65. In contrast, GAD antibodies did not recognize 37,000/40,000 M(r) fragments, and neither GAD isoforms blocked autoantibody binding to precursors of these fragments. The 37,000/40,000 M(r) fragments, but not the 50,000 M(r) fragments, were detected after trypsin treatment of immunoprecipitates from insulinoma cells that lacked expression of major GAD isoforms. Antibodies in IDDM did not bind native or trypsinized islet heat shock proteins. Thus, IDDM patients possess antibodies to GAD, but also distinct antibodies to a 64,000 M(r) protein that is not related to known GAD isoforms or heat shock proteins.
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