کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5509206 | 1538507 | 2017 | 39 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
TNF phase III signalling in tolerant cells is tightly controlled by A20 and CYLD
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کلمات کلیدی
NF-κBIKKBclECLIκBPMSFA20GAPDHTNFAIP3GFPRLATNFLinear Ubiquitin Chain Assembly ComplexcIAP - ciapIκB kinase - IkB kinaseFIV - IVFMAPK - MAPKinflammation - التهاب( توروم) interleukin - اینترلوکینcellular Inhibitor of Apoptosis - بازدارنده سلولی آپوپتوزELISA - تست الیزاEnzyme-linked immunosorbent assay - تست الیزاTolerance - تلرانس Knock-down - دست کشیدنCyld - سیلدtumor necrosis factor - فاکتور نکروز تومورnuclear factor κB - فاکتور هسته ای κBphosphorylated - فسفریلید شدهrelative luciferase activity - فعالیت لوکیفراز نسبیphenylmethylsulfonyl fluoride - فنیل متیل سولفونیل فلورایدLUBAC - لوباکMalt - مالتinhibitor of NF-κB - مهارکننده NF-κBnot significant - مهم نیستknock-out - ناک اوتAntibody - پادتَن یا آنتیبادیRIP - پاره کردنgreen fluorescent protein - پروتئین فلورسنت سبزmitogen activated protein kinase - پروتئین کیناز فعال Mitogen فعال استReceptor interacting protein - پروتئین گیرنده گیرندهenhanced chemoluminescence - چمولومینسانس پیشرفتهglyceraldehyde-3-phosphate dehydrogenase - گلیسرالیدید-3-فسفات دهیدروژناز
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: TNF phase III signalling in tolerant cells is tightly controlled by A20 and CYLD TNF phase III signalling in tolerant cells is tightly controlled by A20 and CYLD](/preview/png/5509206.png)
چکیده انگلیسی
Following the acute phase of an inflammatory reaction, a strictly controlled resolution of inflammation is necessary. A dysregulation of this process leads to hyperinflammation, chronic inflammatory disease, or immune paralysis. Different mechanisms participate in the coordinated termination of the inflammatory process, e.g. the expression of antiinflammatory molecules and different forms of tolerance. To better understand the processes which mediate resolution of TNF-dependent inflammation and induce tolerance, it is necessary to characterize the signal transduction quality during TNF long-term (pre)incubation. Within a time frame from 12 to 48 h, designated as phase III of the TNF response, we measured an ongoing, constitutive activation of TNFR1/NF-κB-dependent pathways in monocytic cells. Phase III signalling which was also named “constitutive signaling in TNF tolerant cells” induces the expression of low- and high-sensitive target genes including A20 which is differentially regulated by transcriptional and proteolytic events. A20 strictly controls TNF long-term constitutive signalling in an IκB kinase complex- and partially RIP-dependent manner supported by adjuvant ABIN1. In addition, CYLD proteins participate in the regulation of this late-phase signal transduction, whereas downstream molecules such as Bcl3 and p50 are not involved. A20 and CYLD are expressed with different mRNA kinetics resulting in a strong or only a modest increase in protein levels, respectively. The identification of mechanisms which contribute to the termination of inflammation will provide additional diagnostic and therapeutic aspects to specifically diagnose certain aspects of inflammation and specifically modulate them.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 37, September 2017, Pages 123-135
Journal: Cellular Signalling - Volume 37, September 2017, Pages 123-135
نویسندگان
Rolf Bikker, Martin Christmann, Katharina PreuÃ, Bastian Welz, Judith Friesenhagen, Oliver Dittrich-Breiholz, René Huber, Korbinian Brand,