Inhibition of rabbit collagenase (matrix metalloproteinase-1; MMP-1) transcription by retinoid receptors: evidence for binding of RARs/RXRs to the -77 AP-1 site through interactions with c-Jun.

Schroen DJ; Brinckerhoff CE

首页> 外文期刊>Journal of Cellular Physiology >Inhibition of rabbit collagenase (matrix metalloproteinase-1; MMP-1) transcription by retinoid receptors: evidence for binding of RARs/RXRs to the -77 AP-1 site through interactions with c-Jun.

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Inhibition of rabbit collagenase (matrix metalloproteinase-1; MMP-1) transcription by retinoid receptors: evidence for binding of RARs/RXRs to the -77 AP-1 site through interactions with c-Jun.

机译：抑制兔胶原酶(矩阵metalloproteinase-1;类维生素a受体:绑定的证据-77年AP-1 rar / rxr网站通过与c-Jun的交互。

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Treatment of synovial fibroblasts with retinoic acid (RA) decreases their expression of collagenase (matrix metalloproteinase-1 or MMP-1), an enzyme that degrades interstitial collagens and contributes to the pathology of rheumatoid arthritis. This inhibition results, at least in part, from RA-induced decreases in the mRNA for the transactivators Fos and Jun (with concominant increases in RAR mRNA) and by sequestration of Fos/Jun by RARs/RXRs. Previously, we provided evidence that retinoid receptors are also present in complexes that bind to fragments of rabbit MMP-1 promoter DNA containing an AP-1 site at -77 (Pan et al., 1995, J. Cell. Biochem., 57:575-589). However, it was unclear whether RARs and retinoid X receptors (RXRs) were binding directly to the DNA or indirectly through another protein. We now use a sensitive MMP-1 promoter/luciferase reporter construct to confirm the transcriptional role of the AP-1 site at -77. In addition, with electrophoretic mobility shift analyses (EMSAs), antibody "supershifts" and DNAase 1 footprinting, we examine the interaction of retinoid receptors and AP-1 protein on the MMP-1 promoter. We demonstrate that RARs, RXRs, and c-Jun form a complex at the AP-1 site in which c-Jun binds directly to the DNA and apparently tethers the retinoid receptors to the complex. We conclude that retinoid receptors/AP-1 protein interactions at the DNA may provide an additional means of controlling collagenase gene transcription by retinoids.

机译：治疗滑膜成纤维细胞与视黄酸(RA)减少他们的表达胶原酶(矩阵metalloproteinase-1或者金属蛋白酶- 1),一种酶,这种酶降解间质胶原蛋白和导致的病理类风湿性关节炎。至少在某种程度上,从RA-induced减少反式激活因子Fos和小君(提交的信使rnaconcominant增加RAR mRNA)rar / rxr封存”丛书/小君。以前,我们提供的证据表明,类维生素a受体也存在于复合物结合的兔子金属蛋白酶- 1启动子片段的DNA包含一个AP-1站点-77 (Pan et al ., 1995年,j .细胞。不清楚rar和类维生素a X受体(rxr)或直接绑定到DNA通过另一个间接的蛋白质。敏感的金属蛋白酶- 1启动子荧光素酶的记者构建以确认的转录作用AP-1网站在-77年。电泳迁移率改变分析(emsa),抗体“supershifts”和DNAase 1足迹,我们检查类维生素a受体之间的相互作用金属蛋白酶- 1启动子和AP-1蛋白质。证明rar, rxr c-Jun形成复杂的AP-1网站c-Jun绑定显然直接DNA和i类维生素a受体的复杂。这类维生素a受体/ AP-1蛋白质相互作用在DNA可能提供额外的手段控制胶原酶基因转录类维生素a。

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《Journal of Cellular Physiology》 |1996年第2期|320-332|共13页
作者
Schroen DJ; Brinckerhoff CE;
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Department of Medicine, Dartmouth Medical School, Hanover, New Hampshire 03755, USA.;

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原文格式 PDF
正文语种英语
中图分类细胞生物学;
关键词
Collagenases; Genetic Transcription; TretinoinDNARetinoidsChromosomal Probesinterstitial collagenaseRetinoid receptorsTranscription Factor AP-1;

机译：胶原酶;基因Probesinterstitial collagenaseRetinoidAP-1 receptorsTranscription因素;

Inhibition of rabbit collagenase (matrix metalloproteinase-1; MMP-1) transcription by retinoid receptors: evidence for binding of RARs/RXRs to the -77 AP-1 site through interactions with c-Jun.

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