Autoantibodies directed against glutamate decarboxylase interfere with glucose‐stimulated insulin secretion in dispersed rat islets
Author:
Affiliation:
1. Department of Medicine University of Washington Seattle Washington USA
2. Department of Anesthesiology and Pain Medicine University of Washington Seattle Washington USA
Funder
National Institute of Diabetes and Digestive and Kidney Diseases
Publisher
Wiley
Subject
Cell Biology,Molecular Biology,Pathology and Forensic Medicine
Link
https://onlinelibrary.wiley.com/doi/pdf/10.1111/iep.12437
Reference63 articles.
1. Phases of type 1 diabetes in children and adolescents
2. Insulin release from mouse islets perifused with serum IgG from newly insulin‐dependent diabetics;Ziegler M;Acta Biol Med Ger,1982
3. Islet cell surface antibodies preferentially inhibit glucose-stimulated insulin release in vitro
4. Two Forms of the ?-Aminobutyric Acid Synthetic Enzyme Glutamate Decarboxylase Have Distinct Intraneuronal Distributions and Cofactor Interactions
5. Pancreatic beta cells express two autoantigenic forms of glutamic acid decarboxylase, a 65-kDa hydrophilic form and a 64-kDa amphiphilic form which can be both membrane-bound and soluble.
Cited by 2 articles. 订阅此论文施引文献 订阅此论文施引文献，注册后可以免费订阅5篇论文的施引文献，订阅后可以查看论文全部施引文献
1. High glutamic acid decarboxylase antibody titers may be associated with a decline in β-cell function over time and future insulin deficiency in latent autoimmune diabetes in adults;Diabetes Research and Clinical Practice;2024-09
2. Significance of Autoantibodies;Neuroimmune Diseases;2024
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