ShanghaiTech University Knowledge Management System
| The tumor suppressor NF2 modulates TEAD4 stability and activity in Hippo signaling via direct interaction | |
| 2024-05-01 | |
| 发表期刊 | JOURNAL OF BIOLOGICAL CHEMISTRY (IF:4.0[JCR-2023],4.4[5-Year]) |
| ISSN | 0021-9258 |
| EISSN | 1083-351X |
| 卷号 | 300期号:5 |
| 发表状态 | 已发表 |
| DOI | 10.1016/j.jbc.2024.107212 |
| 摘要 | As an output effector of the Hippo signaling pathway, the TEAD transcription factor and co-activator YAP play crucial functions in promoting cell proliferation and organ size. The tumor suppressor NF2 has been shown to activate LATS1/2 kinases and interplay with the Hippo pathway to suppress the YAP-TEAD complex. However, whether and how NF2 could directly regulate TEAD remains unknown. We identified a direct link and physical interaction between NF2 and TEAD4. NF2 interacted with TEAD4 through its FERM domain and Cterminal tail and decreased the protein stability of TEAD4 independently of LATS1/2 and YAP. Furthermore, NF2 inhibited TEAD4 palmitoylation and induced the cytoplasmic translocation of TEAD4, resulting in ubiquitination and dysfunction of TEAD4. Moreover, the interaction with TEAD4 is required for NF2 function to suppress cell proliferation. These fi ndings reveal an unanticipated role of NF2 as a binding partner and inhibitor of the transcription factor TEAD, shedding light on an alternative mechanism of how NF2 functions as a tumor suppressor through the Hippo signaling cascade. |
| 关键词 | Acylation Cell signaling Transcription Transcription factors Tumors Coactivators Crucial functions Direct interactions Direct links Hippo pathway Palmitoylation Protein-protein interactions Signalling pathways TEAD4 Tumour suppressor |
| URL | 查看原文 |
| 收录类别 | EI ; SCI |
| 语种 | 英语 |
| 资助项目 | National Key R&D Program of China["2020YFA0803201","2019YFA0802000"] ; National Natural Science Foundation of China["31970672","32270877","32000496","32030025","31625017"] ; China Postdoctoral Science Foundation[2019M662588] |
| WOS研究方向 | Biochemistry & Molecular Biology |
| WOS类目 | Biochemistry & Molecular Biology |
| WOS记录号 | WOS:001345369000001 |
| 出版者 | ELSEVIER |
| EI入藏号 | 20241715952940 |
| EI主题词 | Cell proliferation |
| EI分类号 | 461.1 Biomedical Engineering ; 461.2 Biological Materials and Tissue Engineering ; 461.9 Biology ; 802.2 Chemical Reactions |
| 原始文献类型 | Journal article (JA) |
| 文献类型 | 期刊论文 |
| 条目标识符 | https://kms.shanghaitech.edu.cn/handle/2MSLDSTB/370133 |
| 专题 | 物质科学与技术学院_硕士生 生物医学工程学院_PI研究组_张雷组（生医工） |
| 通讯作者 | Hu, Liqiao |
| 作者单位 | 1.Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China 2.State Key Laboratory of Cell Biology, Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China 3.College of Life Science and Technology, ShanghaiTech University, Shanghai, China 4.The MOE Key Laboratory of Biosystems Homeostasis and Protection and Innovation Center for Cell Signaling Network, Life Sciences Institute, Zhejiang University, Zhejiang, Hangzhou, China 5.Cancer Center, Zhejiang University, Zhejiang, Hangzhou, China 6.School of Life Science, Hangzhou Institute for Advanced Study, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Hangzhou, China |
| 推荐引用方式 GB/T 7714 | Wu, Mengying,Hu, Liqiao,He, Lingli,et al. The tumor suppressor NF2 modulates TEAD4 stability and activity in Hippo signaling via direct interaction[J]. JOURNAL OF BIOLOGICAL CHEMISTRY,2024,300(5). |
| APA | Wu, Mengying.,Hu, Liqiao.,He, Lingli.,Yuan, Liang.,Yang, Lingling.,...&He, Xiaojing.(2024).The tumor suppressor NF2 modulates TEAD4 stability and activity in Hippo signaling via direct interaction.JOURNAL OF BIOLOGICAL CHEMISTRY,300(5). |
| MLA | Wu, Mengying,et al."The tumor suppressor NF2 modulates TEAD4 stability and activity in Hippo signaling via direct interaction".JOURNAL OF BIOLOGICAL CHEMISTRY 300.5(2024). |
| 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 | ||
修改评论
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。