کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10753384 | 1050340 | 2014 | 5 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Association of malectin with ribophorin I is crucial for attenuation of misfolded glycoprotein secretion
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
PBSα1-antitrypsinKDELRibophorin ILys-Asp-Glu-LeuCNx - CNXendo-β-N-acetylglucosaminidase H - Endo-β-N-acetylglucosaminidase HEndo H - اندو هOst - اورتOligosaccharyltransferase - اولیگوساکاریل ترانسفرازendoplasmic reticulum - شبکه آندوپلاسمی Phosphate-buffered saline - محلول نمک فسفات با خاصیت بافریAntibody - پادتَن یا آنتیبادیmisfolded protein - پروتئین غلط شدهcalnexin - کلنکسین
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Association of malectin with ribophorin I is crucial for attenuation of misfolded glycoprotein secretion Association of malectin with ribophorin I is crucial for attenuation of misfolded glycoprotein secretion](/preview/png/10753384.png)
چکیده انگلیسی
We previously demonstrated that malectin associates with ribophorin I, which is a subunit of oligosaccharyltransferase in the endoplasmic reticulum (ER). When malectin and ribophorin I are overexpressed in the ER, secretion of an α1-antitrypsin (AT) variant whose folding is defective, termed null Hong Kong (ATNHK), is decreased. To confirm whether the interaction between malectin and ribophorin I is involved in the decreased secretion of misfolded glycoproteins, we constructed an expression vector encoding truncated malectin, which could not associate with ribophorin I and had an Lys-Asp-Glu-Leu ER-retention sequence at its C-terminus. Expression of wild-type malectin abrogated ATNHK secretion, whereas expression of truncated malectin did not affect ATNHK secretion. Both wild-type and truncated malectin bound to ATNHK, and the level of ATNHK was similar in cells expressing wild-type malectin and those expressing truncated malectin. Furthermore, we previously showed that decreased secretion of misfolded ATNHK by malectin overexpression is restored by treatment with a proteasome inhibitor. These results clearly demonstrate that the association of malectin with ribophorin I is required to capture misfolded glycoproteins and direct them to the degradation pathway.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 454, Issue 3, 21 November 2014, Pages 436-440
Journal: Biochemical and Biophysical Research Communications - Volume 454, Issue 3, 21 November 2014, Pages 436-440
نویسندگان
Koh Takeda, Sheng-Ying Qin, Naoki Matsumoto, Kazuo Yamamoto,