کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3296890 | 1209876 | 2011 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Autophagy, Microbial Sensing, Endoplasmic Reticulum Stress, and Epithelial Function in Inflammatory Bowel Disease
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کلمات کلیدی
NLRUPRATGssRNAXBP1eIF2αS1PAIECGRP78TLRTh17XBP1SAGR2muramyl dipeptideMDPHypomorphicT helper 17MNVNF-κBJnkmTORTNFIBDC/EBP homologous protein - C / EBP پروتئین همولوگc-Jun N-terminal kinase - C-Jun N-terminal kinasesingle-stranded RNA - RNA تک رشته ایAutophagy - اتوفاژیEndoplasmic reticulum stress - استرس شبکه آندوپلاسمیInnate immunity - ایمنی ذاتیinterleukin - اینترلوکینCrohn's disease - بیماری کرونInflammatory bowel disease - بیماریهای التهابی رودهCHOP - تکه کردنToll-like receptor - تیالآرSite-1 protease - سایت پروتئین 1Dendritic cell - سلول دندریتیکeukaryotic initiation factor 2α - عامل آغاز کننده یوکاریوتی 2αtumor necrosis factor - فاکتور نکروز تومورnuclear factor κB - فاکتور هسته ای κBGenome-wide association studies - مطالعات مرتبط با ژنومGWAS - مطالعهٔ همخوانی سراسر ژنومMurine norovirus - نوروویروس موشmammalian target of rapamycin - هدف پستانداران رپامایسینPathogenesis - پاتونزUnfolded protein response - پاسخ پروتئین آشکارglucose-regulated protein 78 - پروتئین تنظیم شده با گلوکز 78PERK - پرکGenetics - ژنتیکUlcerative colitis - کولیت اولسراتیوNod-like receptor - گیرنده Nod مانند
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
بیماریهای گوارشی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Increasing evidence has emerged that supports an important intersection between 3 fundamental cell biologic pathways in the pathogenesis of inflammatory bowel disease. These include the intersection between autophagy, as revealed by the original identification of ATG16L1 and IRGM as major genetic risk factors for Crohn's disease, and intracellular bacterial sensing, as shown by the importance of NOD2 in autophagy induction upon bacterial entry into the cell. A pathway closely linked to autophagy and innate immunity is the unfolded protein response, initiated by endoplasmic reticulum stress due to the accumulation of misfolded proteins, which is genetically related to ulcerative colitis and Crohn's disease (XBP1 and ORMDL3). Hypomorphic ATG16L1, NOD2, and X box binding protein-1 possess the common attribute of profoundly affecting Paneth cells, specialized epithelial cells at the bottom of intestinal crypts involved in antimicrobial function. Together with their functional juxtaposition in the environmentally exposed intestinal epithelial cell, their remarkable functional convergence on Paneth cells and their behavior in response to environmental factors, including microbes, these 3 pathways are of increasing importance to understanding the pathogenesis of inflammatory bowel disease. Moreover, in conjunction with studies that model deficient nuclear factor-κB function, these studies suggest a central role for altered intestinal epithelial cell function as one of the earliest events in the development of inflammatory bowel disease.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Gastroenterology - Volume 140, Issue 6, May 2011, Pages 1738-1747.e2
Journal: Gastroenterology - Volume 140, Issue 6, May 2011, Pages 1738-1747.e2
نویسندگان
Arthur Kaser, Richard S. Blumberg,