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
• 起止时间: 2009 至 2011
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-21550162/
• 关键词: RNA; プロセシング; S1-1; RBM10; 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

(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.

(1) s1-1 抑制抗癌药物诱导的细胞死亡。它调节剪接，并产生抗凋亡的Fas亚型。(2)通过S1-1免疫组化对350个癌组织切片检查S1-1与肿瘤发生的关系。然而，S1-1的表达与癌细胞类型或癌症恶性程度没有相关性。(3)S1-1也是一种转录因子。值得注意的是，S1-1同时调节转录和剪接。(4)在S1-1分子中鉴定出3个核定位序列，以及2个在细胞转录活性降低的情况下将S1-1隔离到S1-1核体中的序列。关于这些发现的手稿正在准备中。

项目成果

2009年春までの担当講座

课程教授至 2009 年春季

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