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DOI | 10.1126/science.aao3048 |
Cancer mutations and targeted drugs can disrupt dynamic signal encoding by the Ras-Erk pathway | |
Bugaj, L. J.1,7; Sabnis, A. J.2,3; Mitchell, A.1,8; Garbarino, J. E.4; Toettcher, J. E.1,9; Bivona, T. G.1,3,5; Lim, W. A.1,3,4,6 | |
2018-08-31 | |
发表期刊 | SCIENCE
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ISSN | 0036-8075 |
EISSN | 1095-9203 |
出版年 | 2018 |
卷号 | 361期号:6405 |
文章类型 | Article |
语种 | 英语 |
国家 | USA |
英文摘要 | The Ras-Erk (extracellular signal-regulated kinase) pathway encodes information in its dynamics; the duration and frequency of Erk activity can specify distinct cell fates. To enable dynamic encoding, temporal informationmust be accurately transmitted from the plasma membrane to the nucleus. We used optogenetic profiling to show that both oncogenic B-Raf mutations and B-Raf inhibitors can cause corruption of this transmission, so that short pulses of input Ras activity are distorted into abnormally long Erk outputs. These changes can reshape downstream transcription and cell fates, resulting in improper decisions to proliferate. These findings illustrate how altered dynamic signal transmission properties, and not just constitutively increased signaling, can contribute to cell proliferation and perhaps cancer, and how optogenetic profiling can dissect mechanisms of signaling dysfunction in disease. |
领域 | 地球科学 ; 气候变化 ; 资源环境 |
收录类别 | SCI-E |
WOS记录号 | WOS:000443547000031 |
WOS关键词 | WILD-TYPE ; FEEDBACK PHOSPHORYLATION ; MAPK PATHWAY ; BRAF ; SPECIFICITY ; INHIBITORS ; ACTIVATION ; MECHANISMS ; TRANSMISSION ; INFORMATION |
WOS类目 | Multidisciplinary Sciences |
WOS研究方向 | Science & Technology - Other Topics |
引用统计 | |
文献类型 | 期刊论文 |
条目标识符 | http://119.78.100.173/C666/handle/2XK7JSWQ/199487 |
专题 | 地球科学 资源环境科学 气候变化 |
作者单位 | 1.Univ Calif San Francisco, Dept Cellular & Mol Pharmacol, San Francisco, CA 94158 USA; 2.Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94158 USA; 3.Univ Calif San Francisco, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA 94158 USA; 4.Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94158 USA; 5.Univ Calif San Francisco, Div Hematol & Oncol, San Francisco, CA 94158 USA; 6.Univ Calif San Francisco, Ctr Syst & Synthet Biol, San Francisco, CA 94158 USA; 7.Univ Penn, Dept Bioengn, Philadelphia, PA 19104 USA; 8.Univ Massachusetts, Sch Med, Program Syst Biol, Worcester, MA 01655 USA; 9.Princeton Univ, Dept Mol Biol, Princeton, NJ 08544 USA |
推荐引用方式 GB/T 7714 | Bugaj, L. J.,Sabnis, A. J.,Mitchell, A.,et al. Cancer mutations and targeted drugs can disrupt dynamic signal encoding by the Ras-Erk pathway[J]. SCIENCE,2018,361(6405). |
APA | Bugaj, L. J..,Sabnis, A. J..,Mitchell, A..,Garbarino, J. E..,Toettcher, J. E..,...&Lim, W. A..(2018).Cancer mutations and targeted drugs can disrupt dynamic signal encoding by the Ras-Erk pathway.SCIENCE,361(6405). |
MLA | Bugaj, L. J.,et al."Cancer mutations and targeted drugs can disrupt dynamic signal encoding by the Ras-Erk pathway".SCIENCE 361.6405(2018). |
条目包含的文件 | 条目无相关文件。 |
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