fragment design x sa的問題，透過圖書和論文來找解法和答案更準確安心。 我們找到下列股價、配息、目標價等股票新聞資訊

1,3-二苯基脲衍生物之合成與抗茲卡病毒活性

為了解決fragment design x sa的問題，作者賴志韋 這樣論述：

Niclosamide是已被許可用於對抗蠕蟲之驅蟲藥物，近期研究指出niclosamide亦具有抗茲卡病毒效果，因此，藉由修飾其結構可發現更具有抗茲卡病毒效果之潛力衍生物，其中，salicylanilide已藉由細胞實驗證實可有效抑制茲卡病毒非結構蛋白NS3與NS2B結合，阻斷病毒RNA複製，進而產生抗病毒效果。Niclosamide與前述衍生物結構上之共通點為同樣具有兩個拉電子基苯環，在這基礎上，本研究篩檢一系列同樣具有兩個拉電子基苯環之1,3-diphenylurea衍生物，衍生物中CN2H4N抗病毒活性大於niclosamide 2倍以上，並發現苯環對位拉電子基會增加抗病毒活性，ure

a linker作用在病毒結合及胞吞作用的構效機制關係。此結果指出CN2H4N等1,3-diphenylurea衍生物為更具有對抗茲卡病毒發展潛力之藥物。

Snail上調FN, LEF, COX2 及 COL1A1基因的分子機轉: Snail轉錄活化間質蛋白的共同模式之建立

為了解決fragment design x sa的問題，作者Ly Minh Tam 這樣論述：

Hepatocellular carcinoma (HCC) progression involves a mechanism known as epithelial mesenchymal transition (EMT). Snail (SNA) is one of the most important transcription factors in EMT because it has the ability to decrease epithelial genes while upregulating mesenchymal genes. Nevertheless, the pro

cesses by which SNA transactivates mesenchymal markers remain unknown. Previously, we established that SNA works in collaboration with SP1 and EGR1 to directly induce ZEB1 and MMP9 transcription. Surprisingly, upstream of the EGR/SP1 overlapping area on promoters, a SNA-binding motif (TCACA) was dis

covered. Hence, the point of this research was to identify whether SNA similarly upregulates four other mesenchymal genes: fibronectin (FN), lymphoid enhancer-binding factor (LEF), collagen type alpha I (COL1A1), and cyclooxygenase 2 (COX2). SNA, as expected, is required for the activity of these me

senchymal markers. By using deletion mapping and site directed mutagenesis in combination with a dual luciferase promoter assay, it was found that the SNA-binding motif and the EGR1/SP1 overlapping area are necessary for transcription of FN, LEF, COL1A1, and COX2 genes elicited by the phorbol ester

tumor promoter 12-O-tetradecanoyl-phorbol 13-acetate (TPA) in HCC340 and HepG2 HCC cells. Furthermore, using ChIP and EMSA, TPA consistently promoted SNA and EGR1/SP1 binding to these mesenchymal genes' key promoter regions. So far, we've determined that six mesenchymal markers are activated by SNA

in the same transcriptional manner. Likewise, a systematic screening exhibited similar sequence structures in the promoter areas of other SNA-induced mesenchymal genes, implying the possibility of developing a universal model for SNA-induced mesenchymal genes. In conclusion, we hypothesized a novel

mechanism by which Snail acts as a positive transcriptional regulatory factor essential for EMT and metastasis of HCC.Keywords: snail, lymphoid enhancer-binding factor, fibronectin, collagen type alpha I, cyclooxygenase 2, HCC, transcription.