کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
1925897 1536427 2010 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
SelK is a novel ER stress-regulated protein and protects HepG2 cells from ER stress agent-induced apoptosis
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
پیش نمایش صفحه اول مقاله
SelK is a novel ER stress-regulated protein and protects HepG2 cells from ER stress agent-induced apoptosis
چکیده انگلیسی

Selenoprotein K (SelK), an endoplasmic reticulum (ER) resident protein, its biological function has been less-well studied. To investigate the role of SelK in the ER stress response, effects of SelK gene silence and ER stress agents on expression of SelK and cell apoptosis in HepG2 cells were studied. The results showed that SelK was regulated by ER stress agents, Tunicamycin (Tm) and β-Mercaptoethanol (β-ME), in HepG2 cells. Moreover, the SelK gene silence by RNA interference could significantly aggravate HepG2 cell death and apoptosis induced by the ER stress agents. These results suggest that SelK is an ER stress-regulated protein and plays an important role in protecting HepG2 cells from ER stress agent-induced apoptosis.

Research highlights
► The expression of SelK is significantly regulated by ER stress inducers in HepG2 cells.
► The SelK gene silence by RNA interference could markedly increase levels of GADD153 expression and caspase-3 activity.
► The SelK gene silence by RNA interference could significantly aggravate HepG2 cell death and apoptosis induced by ER stress.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Archives of Biochemistry and Biophysics - Volume 502, Issue 2, 15 October 2010, Pages 137–143
نویسندگان
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