کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8633246 | 1569053 | 2018 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Up-regulation of Dyrk1b promote astrocyte activation following lipopolysaccharide-induced neuroinflammation
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
علوم غدد
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Up-regulation of Dyrk1b promote astrocyte activation following lipopolysaccharide-induced neuroinflammation Up-regulation of Dyrk1b promote astrocyte activation following lipopolysaccharide-induced neuroinflammation](/preview/png/8633246.png)
چکیده انگلیسی
Astrocytes become activated in response to different stimulation. Dyrk1b is an arginine-directed serine/threonineprotein kinase that is expressed at elevated levels in many cancers but remains unknown in the pathologies of neuroinflammation. In this study, in vivo, we demonstrated that Dyrk1b expression was significantly increased and reached a peak at 12â¯h after LPS injection via Western blot. Double immunofluorescence staining showed that Dyrk1b co-located with GFAP and Ki67. In vitro, the expression of Dyrk1b, Ki67 and cyclinD1 was gradually increased and reached a peak at 12â¯h in a time-dependent manner after 1â¯Î¼g/mL LPS stimulation. Knockdown of Dyrk1b significantly reduced the expression of Ki67 and cyclinD1. In addition, the data exhibited that silenced Dyrk1b decreased the expression of p-STAT3 in primary astrocyte cells, and Dyrk1b interacted with STAT3 in LPS-induced neuroinflammation. In conclusion, these results suggested that Dyrk1b is increased and may play a crucial role in regulating astrocyte cell activation via interact with STAT3 in LPS-induced neuroinflammation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuropeptides - Volume 69, June 2018, Pages 76-83
Journal: Neuropeptides - Volume 69, June 2018, Pages 76-83
نویسندگان
Mingqing He, Jun Gu, Jinzhou Zhu, Xiaoyan Wang, Chengniu Wang, Chengwei Duan, Yingjie Ni, Xiang Lu, Jianzhong Li,