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首页> 外文期刊>Cell biology international. >The effects of WW2/WW3 domains of Smurf2 molecule on TGF-beta signaling and arginase I gene expression
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The effects of WW2/WW3 domains of Smurf2 molecule on TGF-beta signaling and arginase I gene expression

机译:Smurf2分子的WW2 / WW3结构域对TGF-β信号转导和精氨酸酶I基因表达的影响

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Smad ubiquitination regulatory factor 2 (Smurf2) consists of multiple WW domains which can interact with Smad7 molecule and inhibit signaling of transforming growth factor-beta (TGF-) cytokine. Arginase I (ArgI) is one of the main products of TGF- signaling that plays important roles in tumor escape and airway tissue fibrosis and remodeling in asthma. In this study, the effects of TAT fused to WW2/WW3 (TAT-WW2/WW3) recombinant protein on TGF- signaling and ArgI gene expression were evaluated on J774A.1 cell culture. For this purpose, interaction of TAT-WW2/WW3 with Smad7, mRNA expression of ArgI, and phosphorylated Smad3 (P-Smad3) were analyzed in TAT-WW2/WW3-treated J774A.1 cell. The results showed interaction of TAT-WW2/WW3 with Smad7, downregulation of ArgI gene expression (P<0.05), and higher amount of P-Smad3 in the TAT-WW2/WW3-treated cells. In conclusion, we suggest that TAT-WW2/WW3 could interfere with TGF- signaling and reduce ArgI gene expression. Since, ArgI has important effects on tissue remodeling in asthma and cancer progression, so these findings could be used to develop a new approach in the treatment of asthma and cancers.
机译:Smad泛素化调节因子2(Smurf2)由多个WW域组成,可以与Smad7分子相互作用并抑制转化生长因子-β(TGF-)细胞因子的信号传导。精氨酸酶I(ArgI)是TGF-信号传导的主要产物之一,在哮喘的肿瘤逃逸,气道组织纤维化和重塑中起重要作用。在这项研究中,在J774A.1细胞培养上评估了融合至WW2 / WW3(TAT-WW2 / WW3)重组蛋白的TAT对TGF-信号传导和ArgI基因表达的影响。为此,在经过TAT-WW2 / WW3处理的J774A.1细胞中分析了TAT-WW2 / WW3与Smad7的相互作用,ArgI的mRNA表达以及磷酸化的Smad3(P-Smad3)。结果显示,TAT-WW2 / WW3处理的细胞中TAT-WW2 / WW3与Smad7相互作用,ArgI基因表达下调(P <0.05)和P-Smad3含量更高。总之,我们认为TAT-WW2 / WW3可能会干扰TGF-信号传导并降低ArgI基因表达。由于ArgI对哮喘和癌症进展中的组织重塑具有重要影响,因此这些发现可用于开发治疗哮喘和癌症的新方法。

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