• 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

细胞黏附、细胞张力与细胞周期调控。

Cell adhesion, cellular tension, and cell cycle control.

作者信息

Klein Eric A, Yung Yuval, Castagnino Paola, Kothapalli Devashish, Assoian Richard K

机构信息

Department of Pharmacology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.

出版信息

Methods Enzymol. 2007;426:155-75. doi: 10.1016/S0076-6879(07)26008-2.

DOI:10.1016/S0076-6879(07)26008-2
PMID:17697884
Abstract

Cooperative signaling between growth factor receptor tyrosine kinases, integrins, and the actin cytoskeleton is required for activation of the G1-phase cyclin-dependent kinases and progression through G1-phase. Increasing evidence suggests that there is cell type specificity in these cooperative interactions and that the compliance of the underlying substratum can strongly affect adhesion-dependent signaling to the cell cycle. This chapter reviews our current methods for studying how cell type specificity and changes in substratum compliance can contribute to G1-phase cell cycle control. We also describe several of our current analytical procedures.

摘要

生长因子受体酪氨酸激酶、整合素和肌动蛋白细胞骨架之间的协同信号传导是激活G1期细胞周期蛋白依赖性激酶并推动细胞通过G1期所必需的。越来越多的证据表明,这些协同相互作用存在细胞类型特异性,并且潜在基质的顺应性可强烈影响对细胞周期的黏附依赖性信号传导。本章回顾了我们目前用于研究细胞类型特异性和基质顺应性变化如何有助于G1期细胞周期调控的方法。我们还描述了一些我们目前的分析程序。

相似文献

1
Cell adhesion, cellular tension, and cell cycle control.细胞黏附、细胞张力与细胞周期调控。
Methods Enzymol. 2007;426:155-75. doi: 10.1016/S0076-6879(07)26008-2.
2
Regulation of growth factor signaling and cell cycle progression by cell adhesion and adhesion-dependent changes in cellular tension.细胞黏附以及细胞张力中依赖黏附的变化对生长因子信号传导和细胞周期进程的调控。
Cytokine Growth Factor Rev. 2005 Aug-Oct;16(4-5):395-405. doi: 10.1016/j.cytogfr.2005.03.003.
3
Focal adhesion signaling and actin stress fibers are dispensable for progression through the ongoing cell cycle.粘着斑信号传导和肌动蛋白应力纤维对于正在进行的细胞周期进程并非必需。
J Cell Sci. 2007 Jan 1;120(Pt 1):66-76. doi: 10.1242/jcs.03301. Epub 2006 Dec 5.
4
Coordinate signaling by integrins and receptor tyrosine kinases in the regulation of G1 phase cell-cycle progression.整合素与受体酪氨酸激酶的协同信号传导对G1期细胞周期进程的调控
Curr Opin Genet Dev. 2001 Feb;11(1):48-53. doi: 10.1016/s0959-437x(00)00155-6.
5
Disruption of the actin cytoskeleton leads to inhibition of mitogen-induced cyclin E expression, Cdk2 phosphorylation, and nuclear accumulation of the retinoblastoma protein-related p107 protein.肌动蛋白细胞骨架的破坏会导致有丝分裂原诱导的细胞周期蛋白E表达受到抑制、细胞周期蛋白依赖性激酶2(Cdk2)磷酸化以及视网膜母细胞瘤蛋白相关的p107蛋白的核内积聚。
Exp Cell Res. 2000 Aug 25;259(1):35-53. doi: 10.1006/excr.2000.4966.
6
[Dependence of the process leading to phosphorylation of retinoblastoma protein (pRb) on the status of the actin cytoskeleton].[视网膜母细胞瘤蛋白(pRb)磷酸化过程对肌动蛋白细胞骨架状态的依赖性]
Tsitologiia. 1998;40(2-3):172-7.
7
Adhesion-regulated G1 cell cycle arrest in epithelial cells requires the downregulation of c-Myc.上皮细胞中黏附调节的G1期细胞周期停滞需要c-Myc的下调。
Oncogene. 2001 Jul 27;20(33):4554-67. doi: 10.1038/sj.onc.1204609.
8
[The role of the actin cytoskeleton in cell transition through the middle of the G1 phase of the mitotic cycle].
Tsitologiia. 1996;38(7):733-41.
9
Regulation of cell cycle entry and G1 progression by CSF-1.集落刺激因子-1对细胞周期进入和G1期进程的调控
Mol Reprod Dev. 1997 Jan;46(1):11-8. doi: 10.1002/(SICI)1098-2795(199701)46:1<11::AID-MRD3>3.0.CO;2-U.
10
Adhesion, actin cytoskeleton organisation and the spreading of colon adenocarcinoma cells induced by EGF are mediated by alpha2beta1 integrin low clustering through focal adhesion kinase.表皮生长因子(EGF)诱导的结肠腺癌细胞黏附、肌动蛋白细胞骨架组织及细胞铺展是由α2β1整合素通过黏着斑激酶进行低聚簇介导的。
Histochem Cell Biol. 2001 Oct;116(4):337-48. doi: 10.1007/s004180100324.

引用本文的文献

1
Survivin modulates stiffness-induced vascular smooth muscle cell motility.生存素调节硬度诱导的血管平滑肌细胞运动。
APL Bioeng. 2025 Jun 4;9(2):026120. doi: 10.1063/5.0252766. eCollection 2025 Jun.
2
Survivin modulates stiffness-induced vascular smooth muscle cell motility.存活素调节硬度诱导的血管平滑肌细胞运动。
bioRxiv. 2024 Dec 12:2024.12.11.628062. doi: 10.1101/2024.12.11.628062.
3
Mechanosensitive Differentiation of Human iPS Cell-Derived Podocytes.人诱导多能干细胞来源足细胞的机械敏感性分化
Bioengineering (Basel). 2024 Oct 17;11(10):1038. doi: 10.3390/bioengineering11101038.
4
Survivin regulates intracellular stiffness and extracellular matrix production in vascular smooth muscle cells.存活素调节血管平滑肌细胞的细胞内硬度和细胞外基质产生。
APL Bioeng. 2023 Oct 20;7(4):046104. doi: 10.1063/5.0157549. eCollection 2023 Dec.
5
Key role for Rac in the early transcriptional response to extracellular matrix stiffness and stiffness-dependent repression of ATF3.Rac 在细胞外基质刚度的早期转录反应和 ATF3 的刚度依赖抑制中起关键作用。
J Cell Sci. 2023 Oct 1;136(19). doi: 10.1242/jcs.260636. Epub 2023 Oct 12.
6
A machine learning pipeline revealing heterogeneous responses to drug perturbations on vascular smooth muscle cell spheroid morphology and formation.一种机器学习管道揭示了药物扰动对血管平滑肌细胞球体形态和形成的异质反应。
Sci Rep. 2021 Dec 2;11(1):23285. doi: 10.1038/s41598-021-02683-4.
7
Decreased vascular smooth muscle contractility in Hutchinson-Gilford Progeria Syndrome linked to defective smooth muscle myosin heavy chain expression.亨廷顿舞蹈症-吉福德早衰综合征中血管平滑肌收缩力降低与平滑肌肌球蛋白重链表达缺陷有关。
Sci Rep. 2021 May 19;11(1):10625. doi: 10.1038/s41598-021-90119-4.
8
Mechanosensitive smooth muscle cell phenotypic plasticity emerging from a null state and the balance between Rac and Rho.机械敏感性平滑肌细胞表型可塑性源自于无表型状态和 Rac 与 Rho 之间的平衡。
Cell Rep. 2021 Apr 20;35(3):109019. doi: 10.1016/j.celrep.2021.109019.
9
Yap/Taz Deletion in Gli Cell-Derived Myofibroblasts Attenuates Fibrosis.神经胶质瘤细胞衍生的肌成纤维细胞中Yap/Taz缺失可减轻纤维化。
J Am Soc Nephrol. 2017 Nov;28(11):3278-3290. doi: 10.1681/ASN.2015121354. Epub 2017 Aug 2.
10
Apolipoprotein E3 Inhibits Rho to Regulate the Mechanosensitive Expression of Cox2.载脂蛋白E3抑制Rho以调节Cox2的机械敏感性表达。
PLoS One. 2015 Jun 11;10(6):e0128974. doi: 10.1371/journal.pone.0128974. eCollection 2015.