کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10739385 | 1046873 | 2005 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Induction of apoptosis by the overexpression of an alternative splicing variant of mitochondrial thioredoxin reductase
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Mammalian cells harbor two forms of thioredoxin reductase (TrxR), cytosolic TrxR1 and mitochondrial TrxR2, both of which are involved in the redox regulation of cell growth and apoptosis. Furthermore, several alternative splicing variants of TrxR1 and TrxR2 have been identified. However, little remains known with regard to their functions in cells. Here, we report an alternative splicing variant of TrxR2 (TrxR2A), which displays a 3-bp deletion in the coding region and an insertion of 1228 bp in the 3â²-UTR, between the stop codon and the SECIS element, of the TrxR2 cDNA. In order to determine the cellular function of TrxR2A, we established TrxR2A-inducible HeLa cell lines in which TrxR2A transcription was regulated via a Tet-off expression system. We observed that the induction of TrxR2A resulted in increased apoptosis, due to the reduction of NADPH and alterations in cellular ROS levels. These results suggest that TrxR2A may play a vital role in the regulation of TrxR2 and may confer functional complexity onto the thioredoxin system.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 39, Issue 12, 15 December 2005, Pages 1666-1675
Journal: Free Radical Biology and Medicine - Volume 39, Issue 12, 15 December 2005, Pages 1666-1675
نویسندگان
En Young Chang, Seong-Kweon Son, Hyun Sook Ko, Suk-Hwan Baek, Jung Hye Kim, Jae-Ryong Kim,