کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8269593 | 1534963 | 2015 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Role of Auf1 in elimination of oxidatively damaged messenger RNA in human cells
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کلمات کلیدی
DMEMFBSRRM8-oxo-7,8-dihydroguanine - 8-اکسو-7،8-دی هیدروگوانینRNA recognition motif - RNA تشخیص موتیفROS - ROSRNA degradation - تخریب RNAOxidative stress - تنش اکسیداتیوFree radicals - رادیکال آزادTALEN - زبان هاfetal bovine serum - سرم جنین گاوDulbecco’s modified eagle’s medium - محیط عقاب اصلاح شده DulbeccoReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
In aerobically growing cells, in which reactive oxygen species are produced, the guanine base of RNA is oxidized to 8-oxo-7,8-dihydroguanine, which induces alterations in gene expression. Here we show that the human Auf1 protein, also called HNRNPD, binds specifically to RNA containing this oxidized base and may be involved in cellular processes associated with managing the problems caused by RNA oxidation. Auf1-deficient cells were constructed from human HeLa and Nalm-6 lines using two different targeting procedures. Both types of Auf1-deficient cells are viable, but exhibit growth retardation. The stability of messenger RNA for four different housekeeping genes was determined in Auf1-deficient and -proficient cells, treated with or without hydrogen peroxide. The level of oxidized messenger RNA was considerably higher in Auf1-deficient cells than in Auf1-proficient cells. Auf1 may play a role in the elimination of oxidized RNA, which is required for the maintenance of proper gene expression under conditions of oxidative stress.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 79, February 2015, Pages 109-116
Journal: Free Radical Biology and Medicine - Volume 79, February 2015, Pages 109-116
نویسندگان
Takashi Ishii, Hiroshi Hayakawa, Takeshi Sekiguchi, Noritaka Adachi, Mutsuo Sekiguchi,