کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3030387 | 1183202 | 2006 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Characterization of endoplasmic reticulum-associated degradation of a protein S mutant identified in a family of quantitative protein S deficiency
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کلمات کلیدی
PDIERADHEKWGAAFFTripeptidyl peptidase IITPPIIEndo H - اندو هendoglycosidase H - اندوگلیکوزیداز Hendoplasmic reticulum-associated degradation - تداخل وابسته به شبکیه آندوپلاسمیendoplasmic reticulum - شبکه آندوپلاسمی Proteasome - پروتئازومProtein S - پروتئین Sprotein disulfide isomerase - پروتئین دیسولفید ایزومرازhuman embryo kidney - کلیه جنین انسانWheat germ agglutinin - گیاه گندم آگلوتیینین
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
کاردیولوژی و پزشکی قلب و عروق
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Endoglycosidase H digestion and immunofluorescence staining revealed the mutant being retained in the ER. Epoxomicin, a potent and specific proteasome inhibitor, and Ala-Ala-Phe-CH2Cl (AAF), an inhibitor of tripeptidyl peptidase II (TPPII), suppressed the intracellular degradation of the mutant by about 65% and 50%, respectively. When epoxomicin was combined with AAF, the inhibitory effect was substantially enhanced. Although castanospermine, an inhibitor of glucosidases I and II, did not affect the degradation, kifunensine, an inhibitor of ER mannosidase I, suppressed it. Thus, it appears that the Y595C mutant is degraded through more than one pathway of ERAD, including the proteasome-dependent pathway and an alternate proteasome-independent pathway where proteases such as TPPII may be involved. Production of the critical B isoform of Man8GlcNAc2 targets the mutant for ERAD, however, the interaction with calnexin/calreticulin through monoglucosylated oligosaccharides may not be required for the degradation of the mutant.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Thrombosis Research - Volume 117, Issue 3, 2006, Pages 323-331
Journal: Thrombosis Research - Volume 117, Issue 3, 2006, Pages 323-331
نویسندگان
Hiroko Tsuda, Fuminori Tokunaga, Hiroshi Nagamitsu, Takehiko Koide,