کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10814900 | 1058433 | 2014 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
TRAF-mediated modulation of NF-kB AND JNK Activation by TNFR2
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
CrmAcytokine response modifier ATNFdulbecco modified Eagle's mediumTRADDTRAFAIP1TNFRPEIIKKAP-1IκBNF-κBDMEMJnkHEKcIAP - ciapIκB kinase - IkB kinasecellular Inhibitor of Apoptosis - بازدارنده سلولی آپوپتوزApoptosis - خزان یاختهایRank - رتبهTNF receptor associated factor - عامل گیرنده TNFtumor necrosis factor - فاکتور نکروز تومورnuclear factor κB - فاکتور هسته ای κBactivating protein 1 - فعال سازی پروتئین 1inhibitor of NF-κB - مهارکننده NF-κBhemagglutinin - هماگلوتینینFlag - پرچمPolyethylenimine - پلی اتیلنhuman embryonic kidney - کلیه جنین انسانTNF receptor - گیرنده TNFTNF receptors - گیرنده های TNFDeath receptors - گیرنده های مرگreceptor activator of NF-κB - گیرنده گیرنده NF-κB
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: TRAF-mediated modulation of NF-kB AND JNK Activation by TNFR2 TRAF-mediated modulation of NF-kB AND JNK Activation by TNFR2](/preview/png/10814900.png)
چکیده انگلیسی
Tumor Necrosis Factor Receptor 2 (TNFR2) activates transcription factor κB (NF-κB) and c-Jun N-terminal kinase (JNK). Most of the biological activities triggered by TNFR2 depend on the recruitment of TNF Receptor-Associated Factor 2 (TRAF2) to the intracellular region of the receptor. The intracellular region of TNFR2 contains five highly conserved amino acid sequences, three of which appear implicated in receptor signaling. In this work we have studied the interaction of TNFR2 with TRAF proteins as well as the functional consequences of this interaction. We show that TRAF1, TRAF2 and TRAF3 bind to the receptor through two different binding sites located at conserved modules IV and V of its intracellular region, respectively. We also show that TRAF1 and TRAF3 have opposite effects to TRAF2 on NF-κB and JNK activation by TNFR2. Moreover, we show that TNFR2 is able to induce JNK activation in a TRAF2-independent fashion. This new receptor activity relies on a sequence located in the conserved module III. This region is also responsible for the ability of TNFR2 to induce TRAF2 degradation, thus emphasizing the role of conserved module III (amino acids 338-379) on receptor signaling and regulation. We show that only TNFR2 can induce TRAF2 degradation while TRAF1 or TRAF3 is not subjected to this regulatory mechanism and that TRAF1, but not TRAF3, is able to inhibit TRAF2 degradation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 26, Issue 12, December 2014, Pages 2658-2666
Journal: Cellular Signalling - Volume 26, Issue 12, December 2014, Pages 2658-2666
نویسندگان
LucÃa Cabal-Hierro, Montserrat RodrÃguez, Noelia Artime, Julián Iglesias, Lorea Ugarte, Miguel A. Prado, Pedro S. Lazo,