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Proc Natl Acad Sci U S A. 2013 Sep 17;110(38):15169-70. doi: 10.1073/pnas.1314719110. Epub 2013 Sep 10.
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Mechanism for activation of mutated epidermal growth factor receptors in lung cancer.肺癌中突变型表皮生长因子受体的激活机制。
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Cetuximab response of lung cancer-derived EGF receptor mutants is associated with asymmetric dimerization.肺癌衍生表皮生长因子受体突变体对西妥昔单抗的反应与非对称二聚化有关。
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Structure-based network analysis of activation mechanisms in the ErbB family of receptor tyrosine kinases: the regulatory spine residues are global mediators of structural stability and allosteric interactions.基于结构的受体酪氨酸激酶ErbB家族激活机制的网络分析：调节脊柱残基是结构稳定性和变构相互作用的全局介质。
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CUL4A overexpression enhances lung tumor growth and sensitizes lung cancer cells to erlotinib via transcriptional regulation of EGFR.CUL4A过表达通过对表皮生长因子受体（EGFR）的转录调控增强肺肿瘤生长并使肺癌细胞对厄洛替尼敏感。
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RETRACTED: An ATP-competitive inhibitor modulates the allosteric function of the HER3 pseudokinase.撤回：一种ATP竞争性抑制剂调节HER3假激酶的变构功能。
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本文引用的文献

1
Mechanism for activation of mutated epidermal growth factor receptors in lung cancer.肺癌中突变型表皮生长因子受体的激活机制。
Proc Natl Acad Sci U S A. 2013 Sep 17;110(38):E3595-604. doi: 10.1073/pnas.1220050110. Epub 2013 Sep 9.
2
Insights into the aberrant activity of mutant EGFR kinase domain and drug recognition.突变型 EGFR 激酶结构域异常活性及药物识别的研究进展。
Structure. 2013 Feb 5;21(2):209-19. doi: 10.1016/j.str.2012.11.014. Epub 2012 Dec 27.
3
Oncogenic mutations counteract intrinsic disorder in the EGFR kinase and promote receptor dimerization.致癌突变抵消了 EGFR 激酶的固有无序性，并促进了受体二聚化。
Cell. 2012 May 11;149(4):860-70. doi: 10.1016/j.cell.2012.02.063.
4
Mechanics of EGF receptor/ErbB2 kinase activation revealed by luciferase fragment complementation imaging.荧光素酶片段互补成像揭示表皮生长因子受体/ErbB2 激酶的激活机制。
Proc Natl Acad Sci U S A. 2012 Jan 3;109(1):137-42. doi: 10.1073/pnas.1111316109. Epub 2011 Dec 21.
5
Inhibition of the EGF receptor by binding of MIG6 to an activating kinase domain interface.通过MIG6与激活激酶结构域界面结合来抑制表皮生长因子（EGF）受体。
Nature. 2007 Nov 29;450(7170):741-4. doi: 10.1038/nature05998.
6
Structures of lung cancer-derived EGFR mutants and inhibitor complexes: mechanism of activation and insights into differential inhibitor sensitivity.肺癌来源的表皮生长因子受体（EGFR）突变体与抑制剂复合物的结构：激活机制及对抑制剂敏感性差异的见解
Cancer Cell. 2007 Mar;11(3):217-27. doi: 10.1016/j.ccr.2006.12.017.
7
EGF-independent activation of cell-surface EGF receptors harboring mutations found in gefitinib-sensitive lung cancer.在吉非替尼敏感型肺癌中发现的携带突变的细胞表面表皮生长因子（EGF）受体的不依赖EGF激活
Oncogene. 2007 Mar 8;26(11):1567-76. doi: 10.1038/sj.onc.1209957. Epub 2006 Sep 4.
8
An allosteric mechanism for activation of the kinase domain of epidermal growth factor receptor.表皮生长因子受体激酶结构域激活的变构机制。
Cell. 2006 Jun 16;125(6):1137-49. doi: 10.1016/j.cell.2006.05.013.
9
Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain.肺腺癌对吉非替尼或厄洛替尼获得性耐药与表皮生长因子受体（EGFR）激酶结构域的二次突变有关。
PLoS Med. 2005 Mar;2(3):e73. doi: 10.1371/journal.pmed.0020073. Epub 2005 Feb 22.
10
EGF receptor gene mutations are common in lung cancers from "never smokers" and are associated with sensitivity of tumors to gefitinib and erlotinib.表皮生长因子受体（EGF）基因突变在“从不吸烟”者的肺癌中很常见，且与肿瘤对吉非替尼和厄洛替尼的敏感性相关。
Proc Natl Acad Sci U S A. 2004 Sep 7;101(36):13306-11. doi: 10.1073/pnas.0405220101. Epub 2004 Aug 25.

EGFR lung cancer mutants get specialized.

作者信息

Littlefield Peter, Jura Natalia

机构信息

Cardiovascular Research Institute and Department of Cellular and Molecular Pharmacology, University of California, San Francisco, CA 94158.

出版信息

Proc Natl Acad Sci U S A. 2013 Sep 17;110(38):15169-70. doi: 10.1073/pnas.1314719110. Epub 2013 Sep 10.

DOI:10.1073/pnas.1314719110
PMID:24023066
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3780895/
Abstract
摘要