アクセス数 : ?
ダウンロード数 : ?
ID 106361
著者
カノ, シズカ Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School|Student Lab, the University of Tokushima Faculty of Medicine
西田, 憲生 Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School 徳島大学 教育研究者総覧 KAKEN研究者をさがす
ニシヤマ, チヒロ Student Lab, the University of Tokushima Faculty of Medicine
赤池, 瑶子 Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School
カジタ, ケイスケ Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School
クロカワ, ケン Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School
増田, 清士 Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School KAKEN研究者をさがす
桑野, 由紀 Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School 徳島大学 教育研究者総覧 KAKEN研究者をさがす
タナハシ, トシヒト Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School
六反, 一仁 Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School 徳島大学 教育研究者総覧 KAKEN研究者をさがす
キーワード
truncated SRSF3 protein
oxidative stress
cell growth
c-Jun
資料タイプ
学術雑誌論文
抄録
Serine/arginine-rich splicing factor 3 (SRSF3), a member of the SRSF family, plays a wide-ranging role in gene expression. The human SRSF3 gene generates a major mRNA isoform encoding a functional, full-length protein and a PTC-containing isoform (SRSF3-PTC). The latter is expected to be degraded through the nonsense-mediated mRNA decay system. However, it was reported that SRSF3-PTC mRNA was produced under stressful conditions and translated into a truncated SRSF3 protein (SRSF3-TR). To disclose unknown functions of SRSF3-TR, we established Flp-In-293 cells stably expressing SRSF3-TR. The SRSF3-TR-expressing cells increased mRNA and protein levels of positive regulators for G1 to S phase transition (cyclin D1, cyclin D3, CDC25A, and E2F1) and accelerated their growth. c-Jun is required for progression through the G1 phase, the mechanism by which involves transcriptional control of the cyclin D1 gene. We also found that the JUN promoter activity was significantly increased in the Flp-In-293 cells stably expressing SRSF3-TR, compared with mock-transfected control cells. The SRSF3-TR-expressing cells increased c-Jun and Sp-1 levels, which are important for the positive autoregulation and basal transcription of JUN, respectively. Our results suggest that stress-inducible SRSF3-TR may participate in the acceleration of cell growth through facilitating c-Jun-mediated G1 progression under stressful conditions.
掲載誌名
The journal of medical investigation : JMI
ISSN
13431420
cat書誌ID
AA11166929
60
3-4
開始ページ
228
終了ページ
235
並び順
228
発行日
2013-08
EDB ID
フルテキストファイル
言語
eng
著者版フラグ
出版社版
部局
医学系