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ダウンロード数 : ?
ID 83832
著者
赤池, 瑶子 Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School|Student Lab, the University of Tokushima Faculty of Medicine
クロカワ, ケン Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School|Student Lab, the University of Tokushima Faculty of Medicine
カジタ, ケイスケ Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School|Student Lab, the University of Tokushima Faculty of Medicine
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
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
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
Kang, Wan Seung Institute of Complementary and Integrative Medicine, Medical Research Center, Seoul National University
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
srsf1 gene
alternative splicing
premature stop codon
nonsense-mediated mRNA decay
資料タイプ
学術雑誌論文
抄録
The srsf1 gene encodes serine/arginine-rich splicing factor 1 (SRSF1) that participates
in both constitutive and alternative splicing reactions. This gene possesses two
ultraconserved elements in the 3’ untranslated region (UTR). Skipping of an alternative
intron between the two elements has no effect on the protein-coding sequence, but it generates
a premature stop codon (PTC)-containing mRNA isoform, whose degradation is
considered to depend on nonsense-mediated mRNA decay (NMD). However, several cell
lines (HCT116, RKO, HeLa, and WI38 cells) constitutively expressed significant amounts
of the srsf1 PTC variant. HCT116 cells expressed the PTC variant nearly equivalent to the
major isoform that includes the alternative intron in the 3’ UTR. Inhibition of NMD by silencing
a key effecter UPF1 or by treatment with cycloheximide failed to increase amounts
of the PTC variant in HCT116 cells, and the PTC variant was rather more stable than the
major isoform in the presence of actinomycin D. Our results suggest that the original stop
codon may escape from the NMD surveillance even in skipping of the alternative intron.
The srsf1 gene may produce an alternative splice variant having truncated 3’ UTR to relief
the microRNA- and/or RNA-binding protein-mediated control of translation or degradation.
掲載誌名
The journal of medical investigation : JMI
ISSN
13431420
cat書誌ID
AA11166929
58
3-4
開始ページ
180
終了ページ
187
並び順
180
発行日
2011
備考
The journal of medical investigation : http://medical.med.tokushima-u.ac.jp/jmi/index.html
EDB ID
フルテキストファイル
言語
eng
部局
医学系