P2X7 receptor-mediated TG2 externalization: a link to inflammatory arthritis?

被引：10
作者：
Aeschlimann, Daniel [1 ,2 ]
Knauper, Vera [1 ,2 ]
机构：
[1] Cardiff Univ, Sch Dent, Coll Biomed & Life Sci, Matrix Biol & Tissue Repair Res Unit, Heath Pk, Cardiff CF14 4XY, S Glam, Wales
[2] Cardiff Univ, Coll Biomed & Life Sci, Arthrit Res UK Biomech & Bioengn Ctr Excellence, Sir Martin Evans Bldg,Museum Ave, Cardiff CF10 3AX, S Glam, Wales
来源：
AMINO ACIDS | 2017年 / 49卷 / 03期
关键词：
Transglutaminase; P2X7; receptor; Purinergic signaling; Arthritis; Cartilage; Inflammation; Autoimmunity; PROTEIN CROSS-LINKING; RHEUMATOID-ARTHRITIS; TRANSGLUTAMINASE; P2X(7) RECEPTOR; ACTIVATION; DISEASE; GENE; RELEASE; TISSUE; ATP;
D O I：
10.1007/s00726-016-2319-8
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Transglutaminases have important roles in stabilizing extracellular protein assemblies in tissue repair processes but some reaction products can stimulate immune activation, leading to chronic inflammatory conditions or autoimmunity. Exacerbated disease in models of inflammatory arthritis has been ascribed to sustained extracellular enzyme activity alongside formation of select protein modifications. Here, we review the evidence, with a focus on the link between P2X7R signaling and TG2 export, a pathway that we have recently discovered which ties extracellular protein modifications into the danger signal-mediated innate immune response. These recent insights offer new opportunities for therapeutic intervention.
引用
收藏
页码：453 / 460
页数：8
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