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Enzyme meets a surprise target

机译:酶达到了意外的目标

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摘要

Activating mutations in the gene KRAS, which encodes a member of the Ras protein family, are implicated in the development of many human cancers. However, because drugs that effectively treat these cancers by targeting the K-Ras protein have proved difficult to develop, the search for potential therapeutic targets has turned to the proteins that are activated downstream of this oncoprotein. In this issue, Mazur et al. (page 283) identify the enzyme SMYD3 as a protein that has an unanticipated role in the progression of K-Ras-driven cancers in mice. SMYD3, a lysine methyltransferase, is frequently overexpressed in human cancers. Previous work has indicated that the enzyme primarily acts in the nucleus, adding methyl groups to lysine amino-acid residues on histones (proteins that organize DNA into bundles called nucleosomes). To investigate the role of SMYD3 in K-Ras-driven cancers, Mazur and colleagues used several techniques, spanning the gamut from genetically engineered mouse models to screens for SMYD3 protein substrates.
机译:编码Ras蛋白家族成员的基因KRAS中的激活突变与许多人类癌症的发生有关。但是,由于已证明难以开发通过靶向K-Ras蛋白有效治疗这些癌症的药物,因此寻找潜在的治疗靶点已转向了在该癌蛋白下游激活的蛋白。在本期中,Mazur等人。 (第283页)确定了SMYD3酶是一种在小鼠中由K-Ras驱动的癌症进展中未曾预期的作用的蛋白质。 SMYD3是一种赖氨酸甲基转移酶,经常在人类癌症中过表达。先前的工作表明该酶主要作用于细胞核,在组蛋白(将DNA组织成束的蛋白质称为核小体的蛋白质)上的赖氨酸氨基酸残基上添加甲基。为了研究SMYD3在K-Ras驱动的癌症中的作用,Mazur及其同事使用了多种技术,涵盖了从基因工程小鼠模型到SMYD3蛋白底物筛选的整个领域。

著录项

  • 来源
    《Nature》 |2014年第7504期|225-226B1|共3页
  • 作者单位

    Helen Diller Family Comprehensive Cancer Center and the Department of Cell and Molecular Pharmacology, University of California, San Francisco, San Francisco, California 94158, USA;

    Helen Diller Family Comprehensive Cancer Center and the Department of Cell and Molecular Pharmacology, University of California, San Francisco, San Francisco, California 94158, USA;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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  • 正文语种 eng
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