کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5505730 | 1400276 | 2017 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The tubulin deacetylase sirtuin-2 regulates neuronal differentiation through the ERK/CREB signaling pathway
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Modification of microtubule (MT) dynamics is important for diverse aspects of cellular function including differentiation, cargo trafficking, migration, and adhesion. MTs also play a crucial role in the progression of neuronal development. The MT deacetylase Sirtuin 2 (Sirt2) and histone deacetylase 6 (HDAC6) regulate MT dynamics by deacetylating alpha-tubulin (α-tubulin). In this study, we investigated the role of MT deacetylation in the progression of neuronal differentiation. For this, we examined acetylated α-tubulin levels during the differentiation of stem cells into neurons. Acetylated α-tubulin levels were significantly altered during differentiation, and these changes were abolished following treatment with 10 μM AGK2 (Sirt2 inhibitor) or 3 μM tubastatin A (HDAC6 inhibitor). However, neural-specific protein expression (Nestin, NF-M, and MAP-2) was reduced in AGK2-treated hBM-MSCs (AGK-MSCs), but not in tubastatin A-treated hBM-MSCs (Tubastatin A-MSCs). Inhibition of Sirt2 led to a decrease in ERK phosphorylation (p-ERK) level, but HDAC6 inhibition had no such effect. Similar results were obtained for CREB phosphorylation (p-CREB). The results suggest that Sirt2 plays a crucial role in neuronal differentiation via the ERK-CREB signaling pathway.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 482, Issue 1, 1 January 2017, Pages 182-187
Journal: Biochemical and Biophysical Research Communications - Volume 482, Issue 1, 1 January 2017, Pages 182-187
نویسندگان
Sin-Gu Jeong, Goang-Won Cho,