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Apical junction complex proteins and ulcerative colitis: a focus on the PTPRS gene

机译:根尖交界蛋白和溃疡性结肠炎:侧重于PTPRS基因

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Inflammatory bowel disease is a complex multifactorial disease with a strong geneticncomponent. Recent studies have identified innate immunity (NOD2), autophagy (ATG16L1)nand Th17 pathway (IL23R) genes in the pathogenesis of Crohn’s disease. The pathogenesis ofnulcerative colitis (UC) is less clear; however, there is growing evidence that proteins involvednin the apical junction complex are involved in UC. Here we review the up-to-date studies onnthe genetic basis for IBD and explore the newly described UC-associated apical junctionncomplex pointing to a primary defect in barrier defense. We will focus on the PTPRSn(encoding PTPσ) gene and discuss its and other apical junction complex proteins’ role in thenpathogenesis of UC.
机译:炎症性肠病是一种复杂的多因素疾病,具有很强的遗传成分。最近的研究已经在克罗恩病的发病机理中发现了先天免疫(NOD2),自噬(ATG16L1)n和Th17途径(IL23R)基因。溃疡性结肠炎(UC)的发病机制尚不清楚。然而,越来越多的证据表明,涉及到根尖复合体的蛋白质也参与了UC。在这里,我们审查有关IBD的遗传基础的最新研究,并探讨新近描述的UC相关的心尖交界复合体,指出屏障防御的主要缺陷。我们将重点研究PTPRSn(编码PTPσ)基因,并讨论其和其他根尖结复合蛋白在UC发病中的作用。

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