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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ar.js location based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.

以情境式恐懼制約模式解析幼年記憶形成與遠程記憶提取機制

為了解決ar.js location based的問題，作者蔡宗志 這樣論述：

自然遺忘是一種記憶修剪及簡化的方式，以利於長期記憶的儲存。研究記憶如何長期儲存，是一個相當熱門的研究主題 ，其中幼年健忘為一種自然遺忘的模式，為一種研究遠程記憶機制之重要平台。目前文獻上有數個假說用來解釋幼年情境式記憶在成年時無法被提取的原因，但仍未達共識。大腦中海馬迴在情境式記憶之學習中，扮演著關鍵角色。而後壓皮質則與遠程情境式記憶提取有關，與海馬迴有密不可分的相互連結。然而，海馬迴與後壓皮質網絡在幼年健忘及遠程記憶提取中的關聯性則尚未釐清。為了研究幼年的海馬迴在記憶學習時參與的分子機轉，我們首先確認幼年鼠 (出生後20日)相較於成鼠 (出生後60日)表現長期記憶缺陷於物件位置記憶與情境式

恐懼記憶之作業。同時，在低強度學習條件下，幼年鼠海馬迴CA1的神經興奮度低於成年鼠。藉由電生理，幼年鼠的Schaffer Collateral-CA1 突觸的基礎興奮性突觸傳導與早期長期增益現象皆顯著低於成年鼠。反之，幼年鼠則較容易去增益現象。在神經突觸蛋白質的表現量上，幼年鼠海馬迴CA1的NMDA受體的次體GluN2B、PKMζ和PP2B都顯著高於成年鼠。進一步，我們觀察到CaMKII之Thr286自體磷酸化位點、GluA1之Ser831磷酸化位點，以及PKMζ生合成都會在維持早期長期增益現象出現。在單一次高頻電刺激的條件下，幼年鼠都顯著低於成年鼠。再者，我們發現在幼年鼠給予藥物阻斷NMD

A受體的次體GluN2B或PP2B均能有效地改善早期長期增益現象及長期記憶的表現。在神經迴路的研究上，我們也發現海馬迴會投射至後壓皮質，並於遠程情境式記憶提取時提高神經活性在顆粒狀後壓皮質、非顆粒狀後壓皮質、基底外側杏仁核、齒狀迴、外側內嗅皮質與後鼻皮質。再者，透過活化幼年記憶的後壓皮質印痕細胞，可以維持記憶至兩週之久。這代表後壓皮質在遠程記憶有重要角色。為了研究神經迴路於後壓皮質分區在遠程記憶提取之角色，我們使用順向與逆向的病毒標定法。我們確認小鼠的顆粒狀後壓皮質的興奮性神經從第五層投射至海馬迴背側CA1與非顆粒狀後壓皮質的表層。我們發現化學與光遺傳學抑制顆粒狀後壓皮質至CA1路徑，而非透過

顆粒狀後壓皮質至非顆粒狀後壓皮質路徑，則有選擇性參與遠程記憶提取。藉由這一系列的研究，我們提供了早期長期增益效應維持發育不成熟與後壓皮質印痕細胞是與幼年健忘之發源有關性。我們也發現了一個顆粒狀後壓皮質參與遠程恐懼記憶透過至CA1之路徑。本研究，我們提出了一個幼年健忘模式可能是合適的動物模式去研究遺忘跟遠程記憶之機轉。