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由Jun-雌激素受体嵌合体诱导的激素可调节的肿瘤转化。

Hormone-regulatable neoplastic transformation induced by a Jun-estrogen receptor chimera.

作者信息

Kruse U, Iacovoni J S, Goller M E, Vogt P K

机构信息

The Scripps Research Institute, Department of Molecular and Experimental Medicine, BCC239, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.

出版信息

Proc Natl Acad Sci U S A. 1997 Nov 11;94(23):12396-400. doi: 10.1073/pnas.94.23.12396.

Abstract

The v-jun oncogene encodes a nuclear DNA binding protein that functions as a transcription factor and is part of the activator protein 1 complex. Oncogenic transformation by v-jun is thought to be mediated by the aberrant expression of specific target genes. To identify such Jun-regulated genes and to explore the mechanisms by which Jun affects their expression, we have fused the full-length v-Jun and an amino-terminally truncated form of v-Jun to the hormone-binding domain of the human estrogen receptor. The two chimeric proteins function as ligand-inducible transactivators. Expression of the fusion proteins in chicken embryo fibroblasts causes estrogen-dependent transformation.

摘要

v-jun癌基因编码一种核DNA结合蛋白,该蛋白作为转录因子发挥作用,是激活蛋白1复合体的一部分。v-jun介导的致癌转化被认为是由特定靶基因的异常表达介导的。为了鉴定这些由Jun调节的基因,并探索Jun影响其表达的机制,我们已将全长v-Jun和v-Jun的氨基末端截短形式与人雌激素受体的激素结合域融合。这两种嵌合蛋白作为配体诱导的反式激活因子发挥作用。融合蛋白在鸡胚成纤维细胞中的表达导致雌激素依赖性转化。

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本文引用的文献

1
AP-1 function and regulation.活化蛋白-1的功能与调控
Curr Opin Cell Biol. 1997 Apr;9(2):240-6. doi: 10.1016/s0955-0674(97)80068-3.

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