کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3416225 1593693 2016 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
The nuclear protein Sam68 is recruited to the cytoplasmic stress granules during enterovirus 71 infection
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی میکروب شناسی
پیش نمایش صفحه اول مقاله
The nuclear protein Sam68 is recruited to the cytoplasmic stress granules during enterovirus 71 infection
چکیده انگلیسی


• EV71 infection induces SGs formation, and recruits nuclear protein Sam68 into SGs.
• EV71-induced SGs move throughout the cytoplasm in a microtubule-dependent manner.
• These findings may provide novel underlying mechanism for delineating the role of SGs during EV71 infection.

Our previous study found that the nuclear protein, 68-kDa Src-associated in mitosis protein (Sam68), is translocated to the cytoplasm and forms punctate pattern during enterovirus 71 (EV71) infection [Virus Research, 180 (2014), 1–11]. However, the exact function of this punctate pattern in cytoplasm during EV71 infection remains unknown. In this study, we firstly have examined this punctate pattern of Sam68 re-localization in the cytoplasm, and observed the obvious recruitments of Sam68 to the EV71-induced stress granules (SGs). Sam68, belongs to the KH domain family of RNA binding proteins (RBPs), was then confirmed that its KH domain was essential for this recruitment. Nevertheless, Knockdown of Sam68 expression using ShRNA had no effects on SGs assembly, indicating that Sam68 is not a constitutive component of the SGs during EV71 infection. Lastly, we investigated the importance of microtubulin transport to SGs aggregation, and revealed that microtubule depolymerization inhibited SGs formation, suggesting that EV71-induced SGs move throughout the cytoplasm in a microtubule-dependent manner. Taken together, these results illuminated that EV71 infections can induce SGs formation, and Sam68, as a SGs component, migrates alone with SGs dependent on intact microtubule upon the viral infections. These findings may provide novel underlying mechanism for delineating the role of SGs during EV71 infection.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Microbial Pathogenesis - Volume 96, July 2016, Pages 58–66
نویسندگان
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