کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8325535 | 1539946 | 2010 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Differential regulation of CFTRÎF508 degradation by ubiquitin ligases gp78 and Hrd1
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کلمات کلیدی
CFTRgp78HRD1VIMGFPERADRNA interference - RNA تداخل کنندهRNAi - RNA سرکوبگر،RNA مداخلهگر، RNA خاموش کنندهubiquitin conjugating enzyme - ubiquitin conjugating آنزیمubiquitin ligase - ubiquitin لیگازER-Associated Degradation - تخریب ER-Associatedcystic fibrosis transmembrane conductance regulator - رگولاتور رسانایی فرابنفش فیبروز کیستیکendoplasmic reticulum - شبکه آندوپلاسمی Cystic fibrosis - فیبروز کیستیکCue - نشانهwild type - نوع وحشیgreen fluorescent protein - پروتئین فلورسنت سبز
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Differential regulation of CFTRÎF508 degradation by ubiquitin ligases gp78 and Hrd1 Differential regulation of CFTRÎF508 degradation by ubiquitin ligases gp78 and Hrd1](/preview/png/8325535.png)
چکیده انگلیسی
The most common mutation associated with cystic fibrosis is the deletion of phenylalanine 508 of cystic fibrosis transmembrane conductance regulator (CFTRÎF508). This mutation renders otherwise functional protein susceptible to ER-associated degradation (ERAD) and prevents CFTR from exiting the ER and trafficking to the plasma membrane. In this study, we demonstrate that RNAi-mediated silencing of gp78, an established ubiquitin ligase (E3) involved in ERAD, leads to accumulation of CFTRÎF508 protein in cells. gp78 facilitates the degradation of CFTRÎF508 by enhancing both its ubiquitination and interaction with p97/VCP. SVIP, which is the inhibitor of gp78, causes accumulation of CFTRÎF508. We showed that endogenous gp78 co-immunoprecipitates with Hrd1. Furthermore, the results indicate that silencing the expression of another ERAD E3, Hrd1, leads to stabilization of gp78 and decline in gp78 ubiquitination; thereby enhancing CFTRÎF508 degradation. The results support that gp78 is an E3 targeting CFTRÎF508 for degradation and Hrd1 inhibits CFTRÎF508 degradation by acting as an E3 for gp78.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The International Journal of Biochemistry & Cell Biology - Volume 42, Issue 1, January 2010, Pages 167-173
Journal: The International Journal of Biochemistry & Cell Biology - Volume 42, Issue 1, January 2010, Pages 167-173
نویسندگان
Petek Ballar, Ahmet Uygar Ors, Hui Yang, Shengyun Fang,