• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Pseudopodium-enriched atypical kinase 1 regulates the cytoskeleton and cancer progession
【24h】

Pseudopodium-enriched atypical kinase 1 regulates the cytoskeleton and cancer progession

机译：富含伪足蛋白的非典型激酶1调节细胞骨架和癌症进展

获取原文
获取原文并翻译 | 示例
       
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Regulation of the actin-myosin cytoskeleton plays a central role in cell migration and cancer progression. Here, we report the discovery of a cytoskeleton-associated kinase, pseudopodium-enriched atypical kinase 1 (PEAK1). PEAK1 is a 190-kDa nonreceptor tyrosine kinase that localizes to actin filaments and focal adhesions. PEAK1 undergoes Src-induced tyrosine phosphorylation, regulates the p130Cas-Crk-paxillin and Erk signaling pathways, and operates downstream of integrin and epidermal growth factor receptors (EGFR) to control cell spreading, migration, and proliferation. Perturbation of PEAK1 levels in cancer cells alters anchorage-independent growth and tumor progression in mice. Notably, primary and metastatic samples from colon cancer patients display amplified PEAK1 levels in 81% of the cases. Our findings indicate that PEAK1 is an important cytoskel-etal regulatory kinase and possible target for anticancer therapy.
机译：肌动蛋白-肌球蛋白细胞骨架的调节在细胞迁移和癌症进展中起着核心作用。在这里，我们报告发现了细胞骨架相关激酶，富含伪足蛋白的非典型激酶1（PEAK1）。 PEAK1是一个190kDa的非受体酪氨酸激酶，定位于肌动蛋白丝和粘着斑。 PEAK1经历Src诱导的酪氨酸磷酸化，调节p130Cas-Crk-paxillin和Erk信号通路，并在整联蛋白和表皮生长因子受体（EGFR）的下游运行，以控制细胞的扩散，迁移和增殖。癌细胞中PEAK1水平的扰动会改变小鼠中与锚定无关的生长和肿瘤的进展。值得注意的是，来自结肠癌患者的原发性和转移性样品在81％的病例中显示出扩增的PEAK1水平。我们的研究结果表明，PEAK1是重要的细胞骨架调节激酶，可能是抗癌治疗的靶标。

著录项

  • 来源
  • 作者

    Yingchun Wang; rnJonathan A. Kelber; rnHop S. Tran Cao; rnGreg T. Cantin; rnRui Lin; rnWei Wang; Sharmeela Kaushal; rnJeanne M. Bristow; Thomas S. Edgington; rnRobert M. Hoffman; rnMichael Bouvet; John R. Yates III; rnRichard L. Klemk;

  • 作者单位

    Departments of Pathology and University of California, La Jolla, CA 92093 Departments of Moores Cancer Center, University of California, La Jolla, CA 92093;

    rnDepartments of surgery and University of California, La Jolla, CA 92093;

    rnDepartments of Chemical Physiology La Jolla, CA 92037;

    Immunology, The Scripps Research Institute, La Jolla, CA 92037;

    rnDepartments of Pathology and University of California, La Jolla, CA 92093 Departments of Moores Cancer Center, University of California, La Jolla, CA 92093;

    rnDepartments of Pathology and University of California, La Jolla, CA 92093 Departments of Moores Cancer Center, University of California, La Jolla, CA 92093;

    rnDepartments of Moores Cancer Center, University of California, La Jolla, CA 92093;

    rnDepartments of Pathology and University of California, La Jolla, CA 92093 Departments of Moores Cancer Center, University of California, La Jolla, CA 92093;

    rnImmunology, The Scripps Research Institute, La Jolla, CA 92037;

    rnDepartments of surgery and University of California, La Jolla, CA 92093 AntiCancer, Inc., San Diego, CA 92111;

    rnDepartments of Moores Cancer Center, University of California, La Jolla, CA 92093 Departments of surgery and University of California, La Jolla, CA 92093;

    rnDepartments of Chemical Physiology La Jolla, CA 92037;

    rnDepartments of Pathology and University of California, La Jolla, CA 92093 Departments of Moores Cancer Center, University of California, La Jolla, CA 92093;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    cancer; cell migration; phosphoproteomics;

    机译：癌症;细胞迁移;磷酸蛋白质组学;
  • 入库时间 2022-08-18 00:41:23

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号