PR10149_启动子库_赢润生物-中国基因研究资源库
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货号 种属 载体 描述 价格 周期
PR10149 Human pUC57 1500 2-3 周

产品参数

Gene Promoter: Transforming Growth Factor-beta3
Specificity: Ubiquitous
Backbone: pGL3-basic, pUC57, pcDNA3.1-EGFP, ect.

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Description:
TGFβ is the prototype of a large superfamily of multifunctional cytokines that are differentially expressed and function in a wide range of target cells. The autoregulation of TGFβ appears to be mediated through specific sites in the promoter regions of the distinct isoforms. While these sites have been examined for the TGFβ1 promoter, little is known about the relevant regions in the TGFβ3 promoter. The promoter area of the TGFβ3 gene has little structural or functional similarity to the TGFβ1 promoter. Similarly, transcriptional regulation of this gene has significantly diverged from that of the other TGFβs. It has been reported that a region proximal to the TATA box in the 5’-flanking region of the TGFβ3 gene might be important in regulating TGFβ3 expression, but no conclusive studies have defined the critical sites required for TGFβ induction of TGFβ3 expression. Here we have determined that the TGFβ-inducible region of theTGFβ3 promoter contains three transcription factor binding consensus sites: a CRE at –45 to –39 (GACGTCA), an SBE at –49 to –46 (CAGA), and an activator protein-2 (AP-2) site at –57 to –50 (CCCCAGGC). We have investigated the transcriptional regulation of each of these TGFβ3 gene promoter regions in response to TGFβ exposure, and have demonstrated that the CRE site is the critical site. We have also defined the signal transduction pathways mediating TGFβ induction of TGFβ3 secretion, and demonstrate that Smad3 and CREB-1 are the critical transcription factors involved. While we have previouslyshown that JNKs and ERKs were the critical mediators of TGFβ1 production in untransformed epithelial cells, here we show that JNKs and p38, but not PKA and ERKs, are the critical upstream mediators of TGFβ3 production. Our studies provide new insights into the TGFβ auto-feedback regulatory mechanisms that are required for one of the key biological responses to TGFβ, namely, stimulation of its own secretion. In this case, however, the results are specific for production of TGFβ3. Further, our results demonstrate that blocking these critical points reduces TGFβ3 production, and as such, our findings suggest important intervention strategies for controlling tumor growth mediated by excessive tumor cell-secreted TGFβ3 in the tumor microenvironment.


Liu G et al. 2006. Requirement of Smad3 and CREB-1 in mediating transforming growth factor-beta (TGF beta) induction of TGF beta 3 secretion. J Biol Chem. 2006 Oct 6;281(40):29479-90.

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