کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8396547 | 1544153 | 2014 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Intracellular trafficking of Clostridium botulinum C2 toxin
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کلمات کلیدی
GFPClostridium botulinum C2 toxinLAMP2BFAEEA1DAPI4′,6-diamidino-2-phenylindole - 4 '، 6-دیامیدینو-2-فنیلینولDulbecco's modified Eagle Medium - Eagle Medium اصلاح شده Dulbeccoearly endosome antigen 1 - آنتیژن آندوسوم اولیه 1Endocytosis - آندوسیتوز یا درون بریearly endosomes - اندوسوم های اولیهRecycling endosomes - بازیافت آندوسومbafilomycin A1 - بافیلومایسین A1MDCK cell - سلول MDCKendoplasmic reticulum - شبکه آندوپلاسمی late endosomes - پایان آندوسومlysosomal-associated membrane protein 2 - پروتئین غشای مرتبط با لیزوزوم 2green fluorescent protein - پروتئین فلورسنت سبز
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیوشیمی، ژنتیک و زیست شناسی مولکولی (عمومی)
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Intracellular trafficking of Clostridium botulinum C2 toxin Intracellular trafficking of Clostridium botulinum C2 toxin](/preview/png/8396547.png)
چکیده انگلیسی
Clostridium botulinum C2 toxin is a binary toxin composed of an enzymatic component (C2I) and binding component (C2II). The activated binding component (C2IIa) forms heptamers and the oligomer with C2I is taken up by receptor-mediated endocytosis. We investigated the intracellular trafficking of C2 toxin. When MDCK cells were incubated with C2I and C2IIa at 37 °C, C2I colocalized with C2IIa in cytoplasmic vesicles at 5 min, and C2I then disappeared (15 min incubation and later), and C2IIa was observed in the vesicles. Internalized C2I and C2IIa were transported to early endosomes. Some of both components were returned to the plasma membrane through recycling endosomes, whereas the rest of C2IIa was transported to late endosomes and lysosomes for degradation. Bafilomycin A1, an endosomal acidification inhibitor, caused the accumulation of C2IIa in endosomes, and both nocodazole and colchicine, microtubule-disrupting agents, restricted C2IIa's movement in the cytosol. These results indicated that an internalized C2I and C2IIa complex was delivered to early endosomes, and that subsequent delivery of C2I to the cytoplasm occurred in early endosomes. C2IIa was either sent back to the plasma membranes through recycling endosomes or transported to late endosomes and lysosomes for degradation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicon - Volume 82, May 2014, Pages 76-82
Journal: Toxicon - Volume 82, May 2014, Pages 76-82
نویسندگان
Masahiro Nagahama, Chihiro Takahashi, Kouhei Aoyanagi, Ryo Tashiro, Keiko Kobayashi, Yoshihiko Sakaguchi, Kazumi Ishidoh, Jun Sakurai,