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Jun介导的致癌转化:反式激活与同源二聚化的作用

Oncogenic transformation by Jun: role of transactivation and homodimerization.

作者信息

Hartl M, Vogt P K

机构信息

Department of Microbiology, University of Southern California School of Medicine, Los Angeles 90033.

出版信息

Cell Growth Differ. 1992 Dec;3(12):899-908.

PMID:1472470
Abstract

Jun/JunD and Jun/GCN4 chimeras transform chicken embryo fibroblasts and activate the collagenase promoter in these same cells. Individual constructs differ widely in the two activities, and there is no correlation between transformation and transactivation. These results suggest that oncogenic transformation by Jun is not caused merely by an upregulation of AP-1 activity. Jun constructs with a modified dimerization domain allowing only homodimerization are active in transformation and transactivation in chicken embryo fibroblast cultures. Homodimers of Jun therefore transform and transactivate.

摘要

Jun/JunD和Jun/GCN4嵌合体可转化鸡胚成纤维细胞,并在这些相同细胞中激活胶原酶启动子。各个构建体在这两种活性上差异很大,且转化与反式激活之间没有相关性。这些结果表明,Jun介导的致癌转化不仅仅是由AP-1活性上调引起的。具有仅允许同源二聚化的修饰二聚化结构域的Jun构建体在鸡胚成纤维细胞培养物的转化和反式激活中具有活性。因此,Jun的同源二聚体具有转化和反式激活作用。

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