Protein kinase C delta is a substrate of tissue transglutaminase and a novel autoantigen in coeliac disease

被引：3

作者：

Byrne, Greg ^{[1
]}

Freeley, Michael ^{[2
]}

Feighery, Con ^{[3
,4
]}

Whelan, Alex ^{[3
,4
]}

Long, Aideen ^{[2
]}

机构：

[1] Dublin Inst Technol, Sch Biol Sci, Dublin 8, Ireland

[2] Trinity Coll Dublin, Inst Mol Med, Dept Clin Med, Dublin 8, Ireland

[3] St James Hosp, Dept Immunol, Dublin, Ireland

[4] Trinity Coll Dublin, Dublin 8, Ireland

来源：

CLINICAL IMMUNOLOGY | 2013年 / 147卷 / 01期

关键词：

Coeliac disease; Autoantibodies; Tissue transglutaminase; Protein kinase C delta; IGA ANTIBODIES; CANCER CELLS; APOPTOSIS; AUTOANTIBODIES; ACTIN; MICE; AUTOIMMUNITY; ENZYME; DEATH; BETA;

D O I：

10.1016/j.clim.2013.01.007

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

071005 [微生物学]; 100108 [医学免疫学];

摘要：

Post-translational modification of proteins by deamidation or transamidation by tissue transglutaminase (tTG) has been suggested as a possible mechanism for the development of autoimmunity. Sequence analysis of protein kinase C delta (PKC delta) identified an amino acid motif that suggested the possibility that PKC delta was a glutamine substrate of tTG and MALDI-TOF analysis of synthesised peptides from PKC delta proved that this was the case. Polymerisation experiments using recombinant tTG and biotinylated hexapeptide substrate incorporation assays demonstrated that PKC delta is a substrate for tTG-mediated transamidation. Elevated levels of anti-PKG delta antibodies were detected in sera from patients with coeliac disease (p<0.0001) but not from patients with other autoimmune disorders. These data suggest that a subset of patients with coeliac disease produce autoantibodies against PKC delta and that this response may stem from a tTG PKC delta substrate interaction. (C) 2013 Elsevier Inc. All rights reserved.

引用

页码：1 / 8

页数：8

共 39 条

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Transglutaminase catalyzes differential crosslinking of small heat shock proteins and amyloid-β [J].