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FosB的一种可变剪接形式是Fos蛋白转录激活和转化的负调节因子。

An alternative spliced form of FosB is a negative regulator of transcriptional activation and transformation by Fos proteins.

作者信息

Yen J, Wisdom R M, Tratner I, Verma I M

机构信息

Molecular Biology and Virology Laboratory, Salk Institute, San Diego, CA 92186-5800.

出版信息

Proc Natl Acad Sci U S A. 1991 Jun 15;88(12):5077-81. doi: 10.1073/pnas.88.12.5077.

DOI:10.1073/pnas.88.12.5077
PMID:1905017
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC51814/
Abstract

Two forms of FosB transcript and their products can be identified in mouse NIH 3T3 cells following serum induction. The larger RNA codes for a 338-amino acid protein, whereas the smaller RNA results from the removal of an additional 140 nucleotides from FosB mRNA by alternative splicing. This alternative splicing event places a stop codon following the "leucine zipper" region and results in a shorter protein (FosB2) of 237 amino acids that lacks 101 amino acids at the carboxyl terminus. FosB2 is able to form heterodimers with c-Jun and bind to an AP-1 site but is not able to activate the transcription of promoters containing AP-1 sites. Furthermore, FosB2 can not only suppress the transcriptional activation by c-Fos and c-Jun of promoters containing an AP-1 site but also interferes with the transforming potential of viral and cellular Fos proteins. We propose that FosB2 protein functions as a trans-negative regulator.

摘要

血清诱导后,在小鼠NIH 3T3细胞中可鉴定出两种形式的FosB转录本及其产物。较大的RNA编码一种338个氨基酸的蛋白质,而较小的RNA是通过可变剪接从FosB mRNA中去除额外的140个核苷酸产生的。这种可变剪接事件在“亮氨酸拉链”区域之后放置了一个终止密码子,从而产生了一种较短的237个氨基酸的蛋白质(FosB2),该蛋白质在羧基末端缺少101个氨基酸。FosB2能够与c-Jun形成异二聚体并结合到AP-1位点,但不能激活含有AP-1位点的启动子的转录。此外,FosB2不仅可以抑制含有AP-1位点的启动子被c-Fos和c-Jun转录激活,还能干扰病毒和细胞Fos蛋白的转化潜能。我们认为FosB2蛋白起反式负调节因子的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebc7/51814/3d005fdbabe5/pnas01062-0023-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebc7/51814/960e691bc7bf/pnas01062-0021-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebc7/51814/b1e3a269bff2/pnas01062-0022-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebc7/51814/a7a8ef97f707/pnas01062-0022-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebc7/51814/b9e9bd56383c/pnas01062-0022-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebc7/51814/de166bcfb0f3/pnas01062-0022-d.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebc7/51814/c79176e7c55c/pnas01062-0023-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebc7/51814/3d005fdbabe5/pnas01062-0023-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebc7/51814/960e691bc7bf/pnas01062-0021-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebc7/51814/b1e3a269bff2/pnas01062-0022-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebc7/51814/a7a8ef97f707/pnas01062-0022-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebc7/51814/b9e9bd56383c/pnas01062-0022-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebc7/51814/de166bcfb0f3/pnas01062-0022-d.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebc7/51814/c79176e7c55c/pnas01062-0023-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebc7/51814/3d005fdbabe5/pnas01062-0023-b.jpg

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