HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Cai, T. Articles by Notkins, A. L. Search for Related Content PubMed PubMed Citation Articles by Cai, T. Articles by Notkins, A. L. Social Bookmarking                What's this?

Analysis of the Coding and Promoter Regions of the Autoantigen IA-2 in Subjects With and Without Autoantibodies to IA-2

¹ Experimental Medicine Section, Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland
² Department of Pathology, University of Florida, Gainesville, Florida

Despite extensive studies on HLA polymorphism, there have been few, if any, studies on allelic forms or mutations in proteins that serve as autoantigens. The present experiments were designed to look for alterations in the coding and promoter regions of the autoantigen IA-2 in type one (insulin-dependent) diabetic patients with autoantibodies to IA-2 as compared with siblings without diabetes or autoantibodies to IA-2. Genomic DNA was used as a template and was amplified by polymerase chain reaction, with pairs of primers encompassing the promoter region and the 23 exons of the coding region of IA-2. A total of nine nucleotide changes were found in the coding region of the six type 1 diabetic patients; four were silent and five were missense changes, but all occurred in the extracellular domain of IA-2 to which autoantibodies are not directed. Few, if any, changes were found in the 5' upstream (-706 to +135) promoter region. The results of the experiments support the null hypothesis that differences among individuals in the nucleotide and amino acid sequences of the promoter and coding regions of IA-2, respectively, do not account for why some individuals develop autoantibodies to IA-2 and others do not.

CiteULike

Del.icio.us

Digg

Reddit

Technorati

This article has been cited by other articles:

				G. Zhang, H. Hirai, T. Cai, J. Miura, P. Yu, H. Huang, M. R Schiller, W. D Swaim, R. D Leapman, and A. L Notkins RESP18, a homolog of the luminal domain IA-2, is found in dense core vesicles in pancreatic islet cells and is induced by high glucose J. Endocrinol., November 1, 2007; 195(2): 313 - 321. [Abstract] [Full Text] [PDF]

				W. E. Winter, N. Harris, and D. Schatz Immunological Markers in the Diagnosis and Prediction of Autoimmune Type 1a Diabetes Clin. Diabetes, October 1, 2002; 20(4): 183 - 191. [Abstract] [Full Text] [PDF]