KIZ OpenIR  > 科研部门  > 生物毒素与人类疾病(张云)
Cell migration-promoting and apoptosis-inhibiting activities of Bm-TFF2 require distinct structure basis
Yu GY1,2,3; Zhang Y1; Xiang Y1,2; Jiang P1,2; Chen ZM1; Lee WH1; Zhang Y*1; zhangy@mail.kiz.ac.cn
2010
发表期刊BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷号400期号:4页码:724-728
合作性质其它
摘要Human trefoil factors (TFFs) play an important role in wound healing, epithelial restitution and anti-inflammatory effects in the gastrointestinal tract by stimulating cell migration and inhibiting cell apoptosis. In our previous study, Bm-TFF2, an amphibian trefoil factor, which is isolated from the skin secretions of frog Bombina maxima, has much stronger activities than human TFFs. We believe that the expression of the recombinant Bm-TFF2 in vitro is useful to decipher its role in amphibian skin repair. Bm-TFF2 contains 12 cysteine residues and has two TFF-domains. In this study, we expressed full-length of Bm-TFF2 and its single-domain truncations (Bm-IFF2-D1 and Bm-TFF2-D2, each contains a single TFF-domain of Bm-TFF2). The recombinant proteins, including full-length and its single-domain truncations of Bm-TFF2, can promote the migration of human epithelial AGS cells and wound healing of rat intestinal epithelial IEC-6 cells. However, only the full-length of Bm-TFF2, but not its single-domain truncations, can inhibit ceramide-induced apoptosis in AGS cells. In summary, it is the first time to use the recombinant Bm-TFF2 and its truncations to investigate its structure-function relationship. And we report that full-length and each domain of Bm-TFF2 can induce cell migration but only the full-length of Bm-TFF2 can suppress apoptosis, indicating that cell migration-promoting and apoptosis-inhibiting activities of Bm-IFF2 require distinct structure basis.
关键词Bm-tff2 Expression Cell Migration Anti-apoptosis Wound Healing
资助者This work was supported by grants from the National Basic Re- search Program of China (973 Program, 2010CB529800), the Na- tional Science & Technology Major Project (2009ZX09103-147), the Chinese National Natural Science Foundation (30630014, 30670412, 30870304) and the Chinese Academy of Sciences ‘‘Key Research Direction” (KSCX2-YW-R-088). ; This work was supported by grants from the National Basic Re- search Program of China (973 Program, 2010CB529800), the Na- tional Science & Technology Major Project (2009ZX09103-147), the Chinese National Natural Science Foundation (30630014, 30670412, 30870304) and the Chinese Academy of Sciences ‘‘Key Research Direction” (KSCX2-YW-R-088). ; This work was supported by grants from the National Basic Re- search Program of China (973 Program, 2010CB529800), the Na- tional Science & Technology Major Project (2009ZX09103-147), the Chinese National Natural Science Foundation (30630014, 30670412, 30870304) and the Chinese Academy of Sciences ‘‘Key Research Direction” (KSCX2-YW-R-088). ; This work was supported by grants from the National Basic Re- search Program of China (973 Program, 2010CB529800), the Na- tional Science & Technology Major Project (2009ZX09103-147), the Chinese National Natural Science Foundation (30630014, 30670412, 30870304) and the Chinese Academy of Sciences ‘‘Key Research Direction” (KSCX2-YW-R-088).
收录类别SCI
语种英语
资助者This work was supported by grants from the National Basic Re- search Program of China (973 Program, 2010CB529800), the Na- tional Science & Technology Major Project (2009ZX09103-147), the Chinese National Natural Science Foundation (30630014, 30670412, 30870304) and the Chinese Academy of Sciences ‘‘Key Research Direction” (KSCX2-YW-R-088). ; This work was supported by grants from the National Basic Re- search Program of China (973 Program, 2010CB529800), the Na- tional Science & Technology Major Project (2009ZX09103-147), the Chinese National Natural Science Foundation (30630014, 30670412, 30870304) and the Chinese Academy of Sciences ‘‘Key Research Direction” (KSCX2-YW-R-088). ; This work was supported by grants from the National Basic Re- search Program of China (973 Program, 2010CB529800), the Na- tional Science & Technology Major Project (2009ZX09103-147), the Chinese National Natural Science Foundation (30630014, 30670412, 30870304) and the Chinese Academy of Sciences ‘‘Key Research Direction” (KSCX2-YW-R-088). ; This work was supported by grants from the National Basic Re- search Program of China (973 Program, 2010CB529800), the Na- tional Science & Technology Major Project (2009ZX09103-147), the Chinese National Natural Science Foundation (30630014, 30670412, 30870304) and the Chinese Academy of Sciences ‘‘Key Research Direction” (KSCX2-YW-R-088).
文献类型期刊论文
条目标识符http://ir.kiz.ac.cn/handle/152453/6342
专题科研部门_生物毒素与人类疾病(张云)
科研部门_动物模型与人类重大疾病机理重点实验室
通讯作者zhangy@mail.kiz.ac.cn
作者单位1.Key Laboratory of Animal Models and Human Disease Mechanisms of The Chinese Academy of Sciences & Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan 650223, China
2.Graduate School of Chinese Academy of Sciences, Beijing 100049, China
3.Department of Biochemistry, Kunming Medical College, Kunming, Yunnan 650032, China
推荐引用方式
GB/T 7714
Yu GY,Zhang Y,Xiang Y,et al. Cell migration-promoting and apoptosis-inhibiting activities of Bm-TFF2 require distinct structure basis[J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS,2010,400(4):724-728.
APA Yu GY.,Zhang Y.,Xiang Y.,Jiang P.,Chen ZM.,...&zhangy@mail.kiz.ac.cn.(2010).Cell migration-promoting and apoptosis-inhibiting activities of Bm-TFF2 require distinct structure basis.BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS,400(4),724-728.
MLA Yu GY,et al."Cell migration-promoting and apoptosis-inhibiting activities of Bm-TFF2 require distinct structure basis".BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 400.4(2010):724-728.
条目包含的文件
文件名称/大小 文献类型 版本类型 开放类型 使用许可
2010110103.pdf(625KB)期刊论文出版稿开放获取CC BY-NC-SA请求全文
个性服务
推荐该条目
保存到收藏夹
查看访问统计
导出为Endnote文件
谷歌学术
谷歌学术中相似的文章
[Yu GY]的文章
[Zhang Y]的文章
[Xiang Y]的文章
百度学术
百度学术中相似的文章
[Yu GY]的文章
[Zhang Y]的文章
[Xiang Y]的文章
必应学术
必应学术中相似的文章
[Yu GY]的文章
[Zhang Y]的文章
[Xiang Y]的文章
相关权益政策
暂无数据
收藏/分享
所有评论 (0)
暂无评论
 

除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。