• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法，用中文像聊天一样搜索，搜遍4000万医学文献。AI智能推荐，让科研检索更轻松。

立即免费搜索

文件翻译

保留排版，准确专业，支持PDF/Word/PPT等文件格式，支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述，25分钟生成高质量综述，智能提取关键信息，辅助科研写作。

立即免费体验

YAP/TAZ启动并维持雪旺细胞的髓鞘形成。

YAP/TAZ initiate and maintain Schwann cell myelination.

作者信息

Grove Matthew, Kim Hyukmin, Santerre Maryline, Krupka Alexander J, Han Seung Baek, Zhai Jinbin, Cho Jennifer Y, Park Raehee, Harris Michele, Kim Seonhee, Sawaya Bassel E, Kang Shin H, Barbe Mary F, Cho Seo-Hee, Lemay Michel A, Son Young-Jin

机构信息

Shriners Hospitals Pediatric Research Center, Center for Neural Repair, Lewis Katz School of Medicine, Temple University, Philadelphia, United States.

Department of Anatomy and Cell Biology, Lewis Katz School of Medicine, Temple University, Philadelphia, United States.

出版信息

Elife. 2017 Jan 26;6:e20982. doi: 10.7554/eLife.20982.

DOI:10.7554/eLife.20982
PMID:28124973
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5287714/
Abstract

Nuclear exclusion of the transcriptional regulators and potent oncoproteins, YAP/TAZ, is considered necessary for adult tissue homeostasis. Here we show that nuclear YAP/TAZ are essential regulators of peripheral nerve development and myelin maintenance. To proliferate, developing Schwann cells (SCs) require YAP/TAZ to enter S-phase and, without them, fail to generate sufficient SCs for timely axon sorting. To differentiate, SCs require YAP/TAZ to upregulate Krox20 and, without them, completely fail to myelinate, resulting in severe peripheral neuropathy. Remarkably, in adulthood, nuclear YAP/TAZ are selectively expressed by myelinating SCs, and conditional ablation results in severe peripheral demyelination and mouse death. YAP/TAZ regulate both developmental and adult myelination by driving TEAD1 to activate Krox20. Therefore, YAP/TAZ are crucial for SCs to myelinate developing nerve and to maintain myelinated nerve in adulthood. Our study also provides a new insight into the role of nuclear YAP/TAZ in homeostatic maintenance of an adult tissue.

摘要

转录调节因子及强效癌蛋白YAP/TAZ的核排除被认为是成年组织稳态所必需的。在此我们表明，核内YAP/TAZ是外周神经发育和髓鞘维持的关键调节因子。为了增殖，发育中的雪旺细胞（SCs）需要YAP/TAZ进入S期，没有它们，就无法产生足够的雪旺细胞来及时进行轴突分选。为了分化，雪旺细胞需要YAP/TAZ上调Krox20，没有它们，就会完全无法形成髓鞘，导致严重的外周神经病变。值得注意的是，在成年期，核内YAP/TAZ由形成髓鞘的雪旺细胞选择性表达，条件性消融会导致严重的外周脱髓鞘和小鼠死亡。YAP/TAZ通过驱动TEAD1激活Krox20来调节发育和成年期的髓鞘形成。因此，YAP/TAZ对于雪旺细胞形成发育中的神经髓鞘以及在成年期维持有髓神经至关重要。我们的研究还为核内YAP/TAZ在成年组织稳态维持中的作用提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/cdfb3de1b89e/elife-20982-resp-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/7ac331ea94b8/elife-20982-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/849e5310da95/elife-20982-fig1-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/b207e0939045/elife-20982-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/b9d3435a5cfd/elife-20982-fig2-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/4246fc75c4a3/elife-20982-fig2-figsupp2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/8aecd59e85be/elife-20982-fig2-figsupp3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/fec86b8d02b1/elife-20982-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/e8eb7f467f4a/elife-20982-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/af82936232f0/elife-20982-fig4-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/bbaba0f6f98d/elife-20982-fig4-figsupp2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/6f3e62c3cff9/elife-20982-fig4-figsupp3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/4cdede58601b/elife-20982-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/e8234ae23c0e/elife-20982-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/e16021d2841d/elife-20982-fig6-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/2bc9ac8d3721/elife-20982-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/bd3f56c66bb0/elife-20982-fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/e06bc7ec8a14/elife-20982-fig8-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/cdfb3de1b89e/elife-20982-resp-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/7ac331ea94b8/elife-20982-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/849e5310da95/elife-20982-fig1-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/b207e0939045/elife-20982-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/b9d3435a5cfd/elife-20982-fig2-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/4246fc75c4a3/elife-20982-fig2-figsupp2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/8aecd59e85be/elife-20982-fig2-figsupp3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/fec86b8d02b1/elife-20982-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/e8eb7f467f4a/elife-20982-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/af82936232f0/elife-20982-fig4-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/bbaba0f6f98d/elife-20982-fig4-figsupp2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/6f3e62c3cff9/elife-20982-fig4-figsupp3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/4cdede58601b/elife-20982-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/e8234ae23c0e/elife-20982-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/e16021d2841d/elife-20982-fig6-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/2bc9ac8d3721/elife-20982-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/bd3f56c66bb0/elife-20982-fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/e06bc7ec8a14/elife-20982-fig8-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1585/5287714/cdfb3de1b89e/elife-20982-resp-fig1.jpg

相似文献

1
YAP/TAZ initiate and maintain Schwann cell myelination.YAP/TAZ启动并维持雪旺细胞的髓鞘形成。
Elife. 2017 Jan 26;6:e20982. doi: 10.7554/eLife.20982.
2
Axon-dependent expression of YAP/TAZ mediates Schwann cell remyelination but not proliferation after nerve injury.轴突依赖性 YAP/TAZ 表达介导施万细胞髓鞘再生，但不促进神经损伤后的增殖。
Elife. 2020 May 21;9:e50138. doi: 10.7554/eLife.50138.
3
YAP and TAZ control peripheral myelination and the expression of laminin receptors in Schwann cells.YAP和TAZ控制施万细胞的外周髓鞘形成及层粘连蛋白受体的表达。
Nat Neurosci. 2016 Jul;19(7):879-87. doi: 10.1038/nn.4316. Epub 2016 Jun 6.
4
TEAD1 is crucial for developmental myelination, Remak bundles, and functional regeneration of peripheral nerves.TEAD1 对于发育性髓鞘形成、雷马克束和周围神经的功能再生至关重要。
Elife. 2024 Mar 8;13:e87394. doi: 10.7554/eLife.87394.
5
A reciprocal regulatory loop between TAZ/YAP and G-protein Gαs regulates Schwann cell proliferation and myelination.TAZ/YAP 和 G 蛋白 Gαs 之间的相互调节环路调节施万细胞的增殖和髓鞘形成。
Nat Commun. 2017 Apr 26;8:15161. doi: 10.1038/ncomms15161.
6
YAP and TAZ regulate Schwann cell proliferation and differentiation during peripheral nerve regeneration.YAP 和 TAZ 在周围神经再生过程中调节施万细胞的增殖和分化。
Glia. 2021 Apr;69(4):1061-1074. doi: 10.1002/glia.23949. Epub 2020 Dec 18.
7
Programming of Schwann Cells by Lats1/2-TAZ/YAP Signaling Drives Malignant Peripheral Nerve Sheath Tumorigenesis.Lats1/2-TAZ/YAP 信号对许旺细胞的编程驱动恶性外周神经鞘瘤的发生。
Cancer Cell. 2018 Feb 12;33(2):292-308.e7. doi: 10.1016/j.ccell.2018.01.005.
8
TEAD1 is crucial for developmental myelination, Remak bundles, and functional regeneration of peripheral nerves.TEAD1对于周围神经的发育性髓鞘形成、雷马克束和功能再生至关重要。
bioRxiv. 2024 Jan 17:2023.02.27.530298. doi: 10.1101/2023.02.27.530298.
9
YAP and TAZ regulate remyelination in the central nervous system.YAP 和 TAZ 调节中枢神经系统中的髓鞘再生。
Glia. 2024 Jan;72(1):156-166. doi: 10.1002/glia.24467. Epub 2023 Sep 19.
10
YAP/TAZ as therapeutic targets in cancer.YAP/TAZ作为癌症治疗靶点
Curr Opin Pharmacol. 2016 Aug;29:26-33. doi: 10.1016/j.coph.2016.05.002. Epub 2016 Jun 2.

引用本文的文献

1
Mechanosensitive Piezo1 channel: an emerging target in demyelination disease.机械敏感型Piezo1通道：脱髓鞘疾病中的一个新兴靶点。
Front Cell Neurosci. 2025 Jul 9;19:1556892. doi: 10.3389/fncel.2025.1556892. eCollection 2025.
2
Shared Lineage, Distinct Outcomes: Yap and Taz Loss Differentially Impact Schwann and Olfactory Ensheathing Cell Development Without Disrupting GnRH-1 Migration.共同谱系，不同结果：Yap和Taz缺失对施万细胞和嗅鞘细胞发育的影响不同，且不影响GnRH-1迁移。
Glia. 2025 Jul 9. doi: 10.1002/glia.70057.
3
Low-Intensity Ultrasound Stimulates TAZ in Schwann cells.

本文引用的文献

1
Myelinating glia differentiation is regulated by extracellular matrix elasticity.髓鞘形成胶质细胞的分化受细胞外基质弹性的调节。
Sci Rep. 2016 Sep 20;6:33751. doi: 10.1038/srep33751.
2
Optimal myelin elongation relies on YAP activation by axonal growth and inhibition by Crb3/Hippo pathway.最佳髓鞘伸长依赖于轴突生长激活 YAP 以及 Crb3/Hippo 通路抑制。
Nat Commun. 2016 Jul 20;7:12186. doi: 10.1038/ncomms12186.
3
Zeb2 is essential for Schwann cell differentiation, myelination and nerve repair.锌指蛋白2对雪旺细胞的分化、髓鞘形成和神经修复至关重要。
低强度超声刺激雪旺细胞中的TAZ。
bioRxiv. 2025 May 14:2025.05.08.652925. doi: 10.1101/2025.05.08.652925.
4
Tuina promotes nerve myelin regeneration in SNI rats through Piezo1/YAP/TAZ pathway.推拿通过Piezo1/YAP/TAZ通路促进坐骨神经损伤（SNI）大鼠的神经髓鞘再生。
J Orthop Surg Res. 2025 May 12;20(1):454. doi: 10.1186/s13018-025-05794-0.
5
The STRIPAK complex is required for radial sorting and laminin receptor expression in Schwann cells.STRIPAK复合物是施万细胞中径向分选和层粘连蛋白受体表达所必需的。
Cell Rep. 2025 Mar 25;44(3):115401. doi: 10.1016/j.celrep.2025.115401. Epub 2025 Mar 6.
6
Dynamically changing extracellular matrix stiffness drives Schwann cell phenotype.动态变化的细胞外基质硬度驱动雪旺细胞表型。
Matrix Biol Plus. 2024 Dec 31;25:100167. doi: 10.1016/j.mbplus.2024.100167. eCollection 2025 Feb.
7
Physical modulation and peripheral nerve regeneration: a literature review.物理调节与周围神经再生：文献综述
Cell Regen. 2024 Dec 23;13(1):32. doi: 10.1186/s13619-024-00215-9.
8
YAP Signaling in Glia: Pivotal Roles in Neurological Development, Regeneration and Diseases.神经胶质细胞中的YAP信号传导：在神经发育、再生和疾病中的关键作用
Neurosci Bull. 2025 Mar;41(3):501-519. doi: 10.1007/s12264-024-01308-w. Epub 2024 Nov 6.
9
Loss of YAP in Schwann cells improves HNPP pathophysiology.施万细胞中 YAP 的缺失改善了 HNPP 的病理生理学。
Glia. 2024 Nov;72(11):1974-1984. doi: 10.1002/glia.24592. Epub 2024 Jul 11.
10
Immobilized NRG1 Accelerates Neural Crest like Cell Differentiation Toward Functional Schwann Cells Through Sustained Erk1/2 Activation and YAP/TAZ Nuclear Translocation.固定化的神经调节蛋白1通过持续激活Erk1/2和YAP/TAZ核转位加速神经嵴样细胞向功能性雪旺细胞的分化。
Adv Sci (Weinh). 2024 Sep;11(33):e2402607. doi: 10.1002/advs.202402607. Epub 2024 Jul 1.
Nat Neurosci. 2016 Aug;19(8):1050-1059. doi: 10.1038/nn.4321. Epub 2016 Jun 13.
4
Zeb2 recruits HDAC-NuRD to inhibit Notch and controls Schwann cell differentiation and remyelination.Zeb2招募组蛋白去乙酰化酶-核小体重塑去乙酰化酶复合物（HDAC-NuRD）以抑制Notch信号，并控制雪旺细胞的分化和髓鞘再生。
Nat Neurosci. 2016 Aug;19(8):1060-72. doi: 10.1038/nn.4322. Epub 2016 Jun 13.
5
Tead1 regulates the expression of Peripheral Myelin Protein 22 during Schwann cell development.Tead1在雪旺细胞发育过程中调节外周髓磷脂蛋白22的表达。
Hum Mol Genet. 2016 Jul 15;25(14):3055-3069. doi: 10.1093/hmg/ddw158. Epub 2016 Jun 10.
6
YAP and TAZ control peripheral myelination and the expression of laminin receptors in Schwann cells.YAP和TAZ控制施万细胞的外周髓鞘形成及层粘连蛋白受体的表达。
Nat Neurosci. 2016 Jul;19(7):879-87. doi: 10.1038/nn.4316. Epub 2016 Jun 6.
7
YAP/TAZ as therapeutic targets in cancer.YAP/TAZ作为癌症治疗靶点
Curr Opin Pharmacol. 2016 Aug;29:26-33. doi: 10.1016/j.coph.2016.05.002. Epub 2016 Jun 2.
8
Schwann cells-axon interaction in myelination.施万细胞-轴突在髓鞘形成中的相互作用。
Curr Opin Neurobiol. 2016 Aug;39:24-9. doi: 10.1016/j.conb.2016.03.006. Epub 2016 Apr 16.
9
Hippo Pathway in Organ Size Control, Tissue Homeostasis, and Cancer.器官大小调控、组织稳态及癌症中的河马信号通路
Cell. 2015 Nov 5;163(4):811-28. doi: 10.1016/j.cell.2015.10.044.
10
Role of YAP/TAZ in cell-matrix adhesion-mediated signalling and mechanotransduction.YAP/TAZ在细胞-基质黏附介导的信号传导和机械转导中的作用。
Exp Cell Res. 2016 Apr 10;343(1):42-53. doi: 10.1016/j.yexcr.2015.10.034. Epub 2015 Oct 30.