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抑制由抗癌剂诱导的细胞死亡。它调节剪接，并产生抗凋亡Fas亚型。(2)用S1 -1免疫组化法检测350例癌组织切片中S1-1与肿瘤发生的关系。然而，S1-1表达与癌细胞类型或癌症恶性程度无关。(3)S1-1也是一个转录因子。值得注意的是，S1-1调节转录和剪接。(4)在S1-1分子中鉴定了三个核定位序列和两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。目前正在编写关于这些调查结果的报告。

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