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v-src基因产物对转化生长因子β1启动子的转录调控是通过AP-1复合体介导的。

Transcriptional regulation of the transforming growth factor beta 1 promoter by v-src gene products is mediated through the AP-1 complex.

作者信息

Birchenall-Roberts M C, Ruscetti F W, Kasper J, Lee H D, Friedman R, Geiser A, Sporn M B, Roberts A B, Kim S J

机构信息

Division of Cancer Treatment, National Cancer Institute, Frederick Cancer Research Facility, Maryland 21701.

出版信息

Mol Cell Biol. 1990 Sep;10(9):4978-83. doi: 10.1128/mcb.10.9.4978-4983.1990.

DOI:10.1128/mcb.10.9.4978-4983.1990
PMID:2117705
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC361127/
Abstract

Growth factor-independent 32D-src and 32D-abl cell lines, established by infecting the interleukin-3-dependent myeloid precursor cell line (32D-123) with retroviruses containing the src or abl oncogene, were used to study transcriptional regulation of transforming growth factor beta 1 (TGF-beta 1) mRNA. Analysis of different TGF-beta 1 promoter constructs regulated by pp60v-src indicated that sequences responsive to high levels of src induction contain binding sites for AP-1. Both src and serum induced expression of the c-fos and c-jun genes in myeloid cells, resulting in transcriptional activation of the TGF-beta 1 gene. We found that serum treatment increased TGF-beta 1 mRNA levels in 32D-123 cells and that the v-Src protein could replace the serum requirement by stimulating binding to the AP-1 complex of the TGF-beta 1 promoter, thereby mediating the induction of TGF-beta 1 transcription.

摘要

通过用含有src或abl癌基因的逆转录病毒感染白细胞介素-3依赖的髓系前体细胞系（32D-123）建立的生长因子非依赖性32D-src和32D-abl细胞系，被用于研究转化生长因子β1（TGF-β1）mRNA的转录调控。对由pp60v-src调控的不同TGF-β1启动子构建体的分析表明，对高水平src诱导有反应的序列含有AP-1的结合位点。src和血清均可诱导髓系细胞中c-fos和c-jun基因的表达，从而导致TGF-β1基因的转录激活。我们发现血清处理可增加32D-123细胞中TGF-β1 mRNA水平，并且v-Src蛋白可通过刺激与TGF-β1启动子的AP-1复合物结合来替代血清需求，从而介导TGF-β1转录的诱导。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f61/361127/d244efcf3362/molcellb00045-0554-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f61/361127/35dc272e75cb/molcellb00045-0550-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f61/361127/b16bb00696c5/molcellb00045-0551-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f61/361127/f4a395ef386b/molcellb00045-0551-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f61/361127/8942b2a9069f/molcellb00045-0552-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f61/361127/187507b01ab4/molcellb00045-0553-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f61/361127/d244efcf3362/molcellb00045-0554-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f61/361127/35dc272e75cb/molcellb00045-0550-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f61/361127/b16bb00696c5/molcellb00045-0551-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f61/361127/f4a395ef386b/molcellb00045-0551-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f61/361127/8942b2a9069f/molcellb00045-0552-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f61/361127/187507b01ab4/molcellb00045-0553-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f61/361127/d244efcf3362/molcellb00045-0554-a.jpg

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