mnt基因缺失揭示的mnt-myc拮抗作用的证据。

Evidence of mnt-myc antagonism revealed by mnt gene deletion.

作者信息

Hurlin Peter J, Zhou Zi-Qiang, Toyo-Oka Kazuhito, Ota Sara, Walker William L, Hirotsune Shinji, Wynshaw-Boris Anthony

机构信息

Shriners' Hospital for Children, Department of Cell and Developmental Biology, Oregon Health Sciences University, Portland, Oregon USA.

出版信息

Cell Cycle. 2004 Feb;3(2):97-9.

PMID:14712062

Abstract

Myc proteins play a central role in promoting cell proliferation and contribute to a diverse array of cancers. My function appears completely dependent on heterodimerization with Max through related bHLHZip regions. Max interaction with Myc is required for DNA binding at so-called E-box sequences and Myc-dependent transcriptional activation. The repressor with similar DNA binding specificity raised the possibility that Mnt may serve a general role as a Myc antagonist.

摘要

Myc蛋白在促进细胞增殖中起核心作用，并与多种癌症相关。其功能似乎完全依赖于通过相关的bHLHZip区域与Max形成异二聚体。Max与Myc的相互作用是在所谓的E-box序列上进行DNA结合以及Myc依赖性转录激活所必需的。具有相似DNA结合特异性的阻遏物增加了Mnt可能作为Myc拮抗剂发挥一般作用的可能性。