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The splicing factor and diseases caused by its anomaly

The splicing factor and diseases caused by its anomaly
剪接因子及其异常引起的疾病
批准号：
21550162
负责人：
INOUE Akira
金额：
$3.16万
依托单位：
Osaka City University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2009
资助国家：
日本
项目状态：
已结题
起止时间：
2009 至 2011
来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-21550162/
关键词：
RNAプロセシングS1-1RBM10スプライシング制御転写制御アポトーシス関連遺伝子がん危険遺伝子核移行配列S1-1 nuclear body targeting sequenceスプラーシング制御Fas抗がん剤アイソフォーム1と2

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中文摘要
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英文摘要
(1) s1-1 suppressed cell death induced by anticancer agents. It regu-lated splicing, and produced an antiapoptotic Fas isoform.(2) Association of S1-1 with tumorigenesis was examined by S1-1 immunohistochemistry for 350 cancer tissue sections. However, S1-1 expression showed no correlation with cancer cell types or cancer malignancy.(3) S1-1 was also a transcription factor. It is noteworthy that S1-1 regulates both transcription and splicing.(4) Three nuclear localization sequences, and two sequences that sequester S1-1 into S1-1 nuclear bodies under reduced cellular transcriptional activity were identified in the S1-1 molecule. Manuscripts on these findings are in preparation.
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2009年春までの担当講座
课程教授至 2009 年春季
DOI： --
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影响因子： --
作者： []
通讯作者：
Phospho-Ser727 of STAT3 regulates STAT3 activity by enhancing dephosphorylation of phospho-Tyr705 largely through TC45
DOI： 10.1111/j.1365-2443.2011.01575.x
发表时间： 2012-02-01
期刊： GENES TO CELLS
影响因子： 2.1
作者： [Wakahara, Ryohei, Kunimoto, Hiroyuki, Nakajima, Koichi]
通讯作者： Nakajima, Koichi
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