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DNA复制与肿瘤发生的新机制?

New Myc-anisms for DNA replication and tumorigenesis?

作者信息

Lebofsky Ronald, Walter Johannes C

机构信息

Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02446, USA.

出版信息

Cancer Cell. 2007 Aug;12(2):102-3. doi: 10.1016/j.ccr.2007.07.013.

Abstract

The c-Myc proto-oncogene is an essential activator of cell proliferation and one of the genes most commonly deregulated in cancer. Although these activities of c-Myc are thought to result from its function as a transcription factor, the scientific literature contains hints that this is not the whole story. A new paper in Nature by Dominguez-Sola et al. reports the surprising observation that c-Myc promotes DNA replication via a nontranscriptional mechanism, and that c-Myc deregulation causes DNA damage predominately during S phase. These results identify c-Myc as a new DNA replication factor and suggest an alternative model for its role in cell growth and tumorigenesis.

摘要

c-Myc原癌基因是细胞增殖的重要激活因子,也是癌症中最常发生失调的基因之一。尽管c-Myc的这些活性被认为是其作为转录因子的功能所致,但科学文献中也有线索表明并非完全如此。多明格斯-索拉等人在《自然》杂志上发表的一篇新论文报道了一个惊人的发现,即c-Myc通过一种非转录机制促进DNA复制,并且c-Myc失调主要在S期导致DNA损伤。这些结果确定c-Myc为一种新的DNA复制因子,并为其在细胞生长和肿瘤发生中的作用提出了一种替代模型。

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