کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10750219 | 1050296 | 2015 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Lack of GCN5 remarkably enhances the resistance against prolonged endoplasmic reticulum stress-induced apoptosis through up-regulation of Bcl-2 gene expression
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کلمات کلیدی
Bcl-2IRE1inositol-requiring protein 1B-cell lymphoma extra-largeGCN5XBP-1Bcl-xLGRP78C/EBP-homologous protein - C / EBP-homologous proteinER stress - استرس استBax - باکسCHOP - تکه کردنX-box binding protein-1 - جعبه اتصال پروتئین -1saga - حماسهApoptosis - خزان یاختهایendoplasmic reticulum - شبکه آندوپلاسمی activating transcription factor 4 - فعال کردن عامل رونویسی 4activating transcription factor 6 - فعال کردن عامل رونویسی 6B-cell lymphoma 2 - لنفوم سلول B 2Gene targeting - هدف ژنglucose-regulated protein 78 - پروتئین تنظیم شده با گلوکز 78protein kinase RNA-like ER kinase - پروتئین کیناز RNA مانند ER kinasePERK - پرک
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Lack of GCN5 remarkably enhances the resistance against prolonged endoplasmic reticulum stress-induced apoptosis through up-regulation of Bcl-2 gene expression Lack of GCN5 remarkably enhances the resistance against prolonged endoplasmic reticulum stress-induced apoptosis through up-regulation of Bcl-2 gene expression](/preview/png/10750219.png)
چکیده انگلیسی
The endoplasmic reticulum (ER), a complex membrane structure, has important roles in all eukaryotic cells. Catastrophe of its functions would lead to ER stress that causes various diseases such as cancer, neurodegenerative diseases, diabetes and so on. Prolonged ER stress could trigger apoptosis via activation of various signal transduction pathways. To investigate physiological roles of histone acetyltransferase GCN5 in regulation of ER stress, we analyzed responses of homozygous GCN5-deficient DT40 mutants, ÎGCN5, against ER stress. GCN5-deficiency in DT40 caused drastic resistance against apoptosis induced by pharmacological ER stress agents (thapsigargin and tunicamycin). Pharmaceutical analysis using specific Bcl-2 inhibitors showed that the drastic resistance against prolonged ER stress-induced apoptosis is, in part, due to up-regulation of Bcl-2 gene expression in ÎGCN5. These data revealed that GCN5 is involved in regulation of prolonged ER stress-induced apoptosis through controlling Bcl-2 gene expression.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 463, Issue 4, 7 August 2015, Pages 870-875
Journal: Biochemical and Biophysical Research Communications - Volume 463, Issue 4, 7 August 2015, Pages 870-875
نویسندگان
Hidehiko Kikuchi, Futoshi Kuribayashi, Hitomi Mimuro, Shinobu Imajoh-Ohmi, Masami Nakayama, Yasunari Takami, Hideki Nishitoh, Tatsuo Nakayama,