Genomic structure and functional analysis of the MAD related gene.

MAD相关基因的基因组结构和功能分析。

• 批准号: 09470244
• 负责人: TAKENOSHITA Seiichi
• 金额: $ 9.73万
• 依托单位: FUKUSHIMA MEDICAL UNIVERSITY (1999-2000)Gunma University (1997-1998)
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (B).
• 财政年份: 1997
• 资助国家: 日本
• 起止时间: 1997 至 2000
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-09470244/
• 关键词: TGF-β; Smad; Tumor suppressor gene; 増殖因子; 遺伝子診断

The structure of objective genes on the human genome is essential for cancer related gene research grounded in DNA in clinical cancer studies. Since 1997, our research group efforts have : focused on structure decisions of MAD related genes and performed functional analysis to clarify TGF-13 signaling pathways and relation to cancer ; selected the TGF-β RII, Smad2, Smad3, Smad6, Smad7 ; examined all manner of cancer tissue gene abnormalities ; and reported those findings. Currently, the project is summarized as below.1. Presently, the following are registered to EMBL/GenBanK (Data Libraries under Accession Nos.)Smad2 : U78726 to U78733Smad3 : AF025293 to AF025300, AB004922 to AB004930Smad4 : (promoter) : U44378Smad6 : AF041062 to AF041065Smad7 : AF026556 to AF0265592. Among TGF-β signaling pathways analyzed here, confirmed gene mutations in human cancer tissue are Smad4, Smad2, TGF-β RII, and RI only. There are no abnormalities in Smad3, Smad6, and Smad7.

目的基因在人类基因组上的结构对于临床癌症研究中以DNA为基础的癌症相关基因研究是必不可少的。自1997年以来，我们的研究小组致力于以下工作：专注于MAD相关基因的结构决定并进行功能分析，以阐明转化生长因子-13信号通路及其与癌症的关系；选择转化生长因子-βRII、Smad2、Smad3、Smad6、Smad7；检测各种癌症组织基因异常；并报告这些发现。目前，该项目总结如下1.目前，以下序列已注册到EMBL/GenBank(数据库登录号)Smad2：U78726至U78733Smad3：AF025293至AF025300，AB004922至AB004930Smad4：(启动子)：U44378Smad6：AF041062至AF041065Smad7：AF026556至AF0265592。在本文分析的转化生长因子-β信号通路中，在人类肿瘤组织中证实的基因突变只有Smad4、Smad2、转化生长因子-βRII和RI。Smad3、Smad6和Smad7均未见异常。

项目成果

Takenoshita S, et al.: "Absence of mutations in the transforming growth factor-beta type II receptor in sporadic lung cancers with microsatellite instability and rare H-ras1 alleles."Carcinogenesis. 18:. 1427-1429 (1997)

Takenoshita S 等人：“具有微卫星不稳定性和罕见 H-ras1 等位基因的散发性肺癌中转化生长因子-β II 型受体不存在突变。”致癌作用。

Miyazono K.: "Positive and negative regulation of TGF-beta signaling."J.Cell Sci.(Review). 113(pt7). 1101-1109 (2000)

Miyazono K.：“TGF-β 信号传导的正向和负向调节。”J.Cell Sci.（评论）。

Takenoshita S,et al.: "Absence of mutation in the analysisi of coding sequences of the entire transforming growth factor beta type II receptor gene in sporadic humangastric cancer using genomic DNA and intron primers." Oncol Rep. 5(1). 77-80 (1998)

Takenoshita S 等人：“使用基因组 DNA 和内含子引物对散发性人类胃癌中整个转化生长因子 β II 型受体基因的编码序列进行分析，发现不存在突变。”

Takenoshita S, et al.: "Characterization of MADR2/Smad2 gene,a human Mad homolog responsible for transforming growth factor-β and activin signal transduction pathway." Genomics. (in press). (1998)

Takenoshita S 等人：“MADR2/Smad2 基因的表征，该基因是负责转化生长因子-β 和激活素信号转导途径的人类 Mad 同源物”（正在出版）。

Yoshida Y, et al.: "Negative Regulation of BMP/Smad Signaling by Tob in Osteoblasts."Cell. 103(7). 1085-1097 (2000)

Yoshida Y 等人：“成骨细胞中 Tob 对 BMP/Smad 信号传导的负调节”细胞。