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本文引用的文献

1
Sos-mediated cross-activation of wild-type Ras by oncogenic Ras is essential for tumorigenesis.Sos 通过癌基因 Ras 介导的野生型 Ras 交叉激活对于肿瘤发生是必不可少的。
Nat Commun. 2012;3:1168. doi: 10.1038/ncomms2173.
2
Oncogenic and wild-type Ras play divergent roles in the regulation of mitogen-activated protein kinase signaling.致癌性和野生型 Ras 在调节有丝分裂原激活的蛋白激酶信号转导中发挥不同的作用。
Cancer Discov. 2013 Jan;3(1):112-23. doi: 10.1158/2159-8290.CD-12-0231. Epub 2012 Oct 25.
3
Discovery of small molecules that bind to K-Ras and inhibit Sos-mediated activation.发现与K-Ras结合并抑制Sos介导激活的小分子。
Angew Chem Int Ed Engl. 2012 Jun 18;51(25):6140-3. doi: 10.1002/anie.201201358. Epub 2012 May 8.
4
Small-molecule ligands bind to a distinct pocket in Ras and inhibit SOS-mediated nucleotide exchange activity.小分子配体结合到 Ras 中的一个独特口袋中,抑制 SOS 介导的核苷酸交换活性。
Proc Natl Acad Sci U S A. 2012 Apr 3;109(14):5299-304. doi: 10.1073/pnas.1116510109. Epub 2012 Mar 19.
5
Ras history: The saga continues.Ras的历程:传奇仍在继续。
Small GTPases. 2010 Jul;1(1):2-27. doi: 10.4161/sgtp.1.1.12178.
6
Tumour maintenance is mediated by eNOS.肿瘤维持由内皮型一氧化氮合酶介导。
Nature. 2008 Apr 3;452(7187):646-9. doi: 10.1038/nature06778. Epub 2008 Mar 16.
7
Wildtype Kras2 can inhibit lung carcinogenesis in mice.野生型Kras2可抑制小鼠肺癌发生。
Nat Genet. 2001 Sep;29(1):25-33. doi: 10.1038/ng721.
8
Identification of residues critical for Ras(17N) growth-inhibitory phenotype and for Ras interaction with guanine nucleotide exchange factors.鉴定对Ras(17N)生长抑制表型以及对Ras与鸟嘌呤核苷酸交换因子相互作用至关重要的残基。
Mol Cell Biol. 1994 Feb;14(2):1113-21. doi: 10.1128/mcb.14.2.1113-1121.1994.
9
Inhibition of NIH 3T3 cell proliferation by a mutant ras protein with preferential affinity for GDP.对GDP具有优先亲和力的突变型ras蛋白对NIH 3T3细胞增殖的抑制作用。
Mol Cell Biol. 1988 Aug;8(8):3235-43. doi: 10.1128/mcb.8.8.3235-3243.1988.

突变型和野生型 Ras:癌症的共犯。

Mutant and wild-type Ras: co-conspirators in cancer.

机构信息

Curriculum in Genetics and Molecular Biology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA.

出版信息

Cancer Discov. 2013 Jan;3(1):24-6. doi: 10.1158/2159-8290.CD-12-0521.

DOI:10.1158/2159-8290.CD-12-0521
PMID:23319767
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3808242/
Abstract

Although the functional interplay between mutant and wild-type Ras in driving tumor initiation and growth has been described, a clear picture of the precise ramifications and mechanisms of this association remains elusive, sometimes with conflicting conclusions. A report in this issue of Cancer Discovery tackles this question, which may have important implications for therapeutic strategies to block mutant Ras for cancer treatment.

摘要

虽然已经描述了突变型和野生型 Ras 之间的功能相互作用在驱动肿瘤起始和生长中的作用,但这种关联的确切后果和机制仍不明确,有时甚至得出相互矛盾的结论。本期《癌症发现》杂志上的一篇报道解决了这个问题,这对于阻止突变型 Ras 用于癌症治疗的治疗策略可能具有重要意义。