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| 1 | Direct regulation of interleukin-6 expression by Notch signaling in macrophages显示文摘Interleukin-6 (IL-6 ) 是一多种,支持 inflammatory cytokine 由房间的各种各样的类型生产了,包括巨噬细胞。在 IL-6 基因倡导者区域以内, CBF1/Su (H)/Lag-1 (CSL ) 的签名绑定主题,在表明小径的槽口的关键 DNA 有约束力的蛋白质,被识别并且发现了与一致重叠原子因素(NF )-κB-binding 地点。槽口发信号高度被保存并且在有免疫力的房间涉及生物功能的规定。在这研究,我们调查了槽口在鼠科的巨噬细胞在 IL-6 抄本的规定发信号的角色。Notch1 蛋白质层次和劈开的 Notch1 (Val1744 ) 的外观的 upregulation 在鼠科的主要骨头与增加的 IL-6 mRNA 表示层次相关很好导出髓的巨噬细胞(BMMφ) 在由和 interferon-gamma 的 lipopolysaccharide (LPS ) 的激活以后(IFN-γ) 。BMMφ 的处理;与 γ压制槽口发信号的 transduction 的 -secretase 禁止者 IL-CHO 在 IL-6 mRNA 的水平和 IL-6 的数量导致了部分减少生产的蛋白质。相反,组成地激活的细胞内部的 Notch1 蛋白质的 overexpression (N 在 RAW264.7 像巨噬细胞的房间线的 IC ) 与空向量控制比在房间 transfected 导致了显著地更高的 IL-6 抄本表示层次。NF-κ B 禁止者完全废除了 mRNA 表示由 N IC 。用 anti-Notch1 抗体的染色质 immunoprecipitation (薄片) 证明 Notch1 在 LPS/IFN-γ 激活的 RAW264.7 房间与 IL-6 倡导者被联系;然而并非在 unstimulated 房间。一起拿,这些结果强烈建议 Notch1 断然经由 NF-κ 调整 IL-6 表示;在激活的巨噬细胞的 B。 | Wipawee Wongchana Tanapat Palaga | 2012 | Cellular & Molecular Immunology2012，9，2： | 15 |
| 2 | Increased ATG5-ATG12 in hepatitis B virus-associated hepatocellular carcinoma and their role in apoptosis显示文摘AIM To investigate autophagy-related genes, particularly ATG12, in apoptosis and cell cycle in hepatitis B virus(HBV)-associated hepatocellular carcinoma(HCC) and non-HBV-HCC cell lines.METHODS The expression of autophagy-related genes in HBVassociated hepatocellular carcinoma and non-HBV-HCC cell lines and human liver tissues was examined by quantitative real-time reverse transcriptase-polymerase chain reaction(q RT-PCR) and western blotting. The silencing of target genes was used to examine the function of various genes in apoptosis and cell cycle progression. RESULTS The expression of autophagy related genes ATG5, ATG12, ATG9 A and ATG4 B expression was analyzed in Hep G2.2.15 cells and compared with Hep G2 and THLE cells. We found that ATG5 and ATG12 m RNA expression was significantly increased in Hep G2.2.15 cells compared to HepG 2 cells(P < 0.005). Moreover, ATG5-ATG12 protein levels were increased in tumor liver tissues compared to adjacent non-tumor tissues mainly from HCC patients with HBV infection. We also analyzed the function of ATG12 in cell apoptosis and cell cycle progression. The percentage of apoptotic cells increased by 11.4% in ATG12-silenced Hep G2.2.15 cells(P < 0.005) but did not change in ATG12-silenced HepG 2 cells under starvation with Earle's balanced salt solution. However, the combination blockade of Notch signaling and ATG12 decreased the apoptotic rate of HepG 2.2.15 cells from 55.6% to 50.4%(P < 0.05). CONCLUSION ATG12 is important for HBV-associated apoptosis and a potential drug target for HBV-HCC. Combination inhibition of ATG12/Notch signaling had no additional effect on HepG 2.2.15 apoptosis. | Areerat Kunanopparat Ingorn Kimkong Tanapat Palaga Pisit Tangkijvanich Boonchoo Sirichindakul Nattiya Hirankarn | 2016 | World Journal of Gastroenterology2016，22，37： | 11 |
| 3 | Delta-like ligand 4 in hepatocellular carcinoma intrinsically promotes tumour growth and suppresses hepatitis B virus replication显示文摘AIM To investigate the role of Delta-like ligand 4(DLL4) on tumour growth in hepatitis B virus(HBV)-associated hepatocellular carcinoma(HCC) in vivo.METHODS We suppressed DLL4 expression in an HBV expressing HCC cell line, HepG2.2.15 and analysed the growth ability of cells as subcutaneous tumours in nude mice. The expression of tumour angiogenesis regulators, VEGF-A and VEGF-R2 in tumour xenografts were examined by western blotting. The tumour proliferation and neovasculature were examined by immunohistochemistry. The viral replication and viral protein expression were measured by quantitative PCR and western blotting, respectively.RESULTS Eighteen days after implantation, tumour volume in mice implanted with sh DLL4 HepG2.2.15 was significantly smaller than in mice implanted with control HepG2.2.15(P < 0.0001). The levels of angiogenesis regulators, VEGF-A and VEGF-R2 were significantly decreased in implanted tumours with suppressed DLL4 compared with the control group(P < 0.001 and P < 0.05, respectively). Furthermore, the suppression of DLL4 expression in tumour cells reduced cell proliferation and the formation of new blood vessels in tumours. Unexpectedly, increased viral replication was observed after suppression of DLL4 in the tumours.CONCLUSION This study demonstrates that DLL4 is important in regulating the tumour growth of HBV-associated HCC as well as the neovascularization and suppression of HBV replication. | Areerat Kunanopparat Jiraphorn Issara-Amphorn Asada Leelahavanichkul Anapat Sanpavat Suthiluk Patumraj Pisit Tangkijvanich Tanapat Palaga Nattiya Hirankarn | 2018 | World Journal of Gastroenterology2018，24，34： | 3 |
| 4 | TCR-mediated Notch signaling regulates proliferation and IFN-γ production in peripheral T cells显示文摘 | Palaga T Miele L Golde TE | 2003 | J Immunol2003，171，6： | 1 |
| 5 | Notch signaling isactivated by TLR stimulation and regulates macrophage functions显示文摘 | Palaga T Buranaruk C Rengpipat S | 2008 | Eur J Immunol2008，38，1： | 1 |
| 6 | TCR-mediated Notch signaling regulates proliferation and IFN-gamma produc- tion in peripheral T cells 显示文摘 | Palaga T Miele L Golde TE | 2003 | J Immunol2003，171，6： | 1 |
| 7 | TCR-mediated Notch signaling regulates proliferation and IFN-gamma production in peripheral T cells显示文摘 | Palaga T Miele L Golde T E et a1 | 2003 | J lmmunol2003，171，6： | 1 |
| 8 | Inhibition of gamma-secre- tase affects proliferation of leukemia and hepatoma cell lines through Notch signaling 显示文摘 | Suwanjunee S Wongchana W Palaga T | 2008 | Anticancer Drugs2008，19，5： | 1 |
| 9 | TCR-mediated Notch signaling regulates proliferation and IFN-gamma production in peripheral T cells显示文摘 | Palaga T Miele L Golde TE | 2003 | J Immuno12003，171，6： | 1 |
| 10 | Enhancement of immune response to a DNA vaccine against Myeobacterium tuberculosis Ag85B by incorporation of an autuphagy inducing system显示文摘 | Meerak J WaniehweeharungnJang SP Palaga T | 2013 | Vaeeine2013，31，5： | 1 |
| 11 | INHIBITION OF NITRIC OXIDE PRODUCTION IN THE MACROPHAGE-LIKE RAW 264.7 CELL LINE BY PROTEIN FROM THE RHIZOMES OF ZINGIBERACEAE PLANTS显示文摘 | C. Chantaranothai T. Palaga A. Karnchanatat P. Sangvanich | 2013 | Preparative Biochemistry and Biotechnology2013，，： | 1 |
| 12 | Notch signaling is activated by TLR stimulation and regulates macrophage functions显示文摘 | Palaga T Buranaruk C Rengpipat S | 2007 | Eur J Immunol2007，38，1： | 1 |
| 13 | Notch signaling is activated by TLR stimulation and regulates macrophage functions显示文摘 | PALAGA T BURANARUK C RENGPIPAT S | 2008 | Eur J Immunol2008，38，： | 1 |
| 14 | Inhibition of gamma-secretase affects proliferation of leukemia and hepatoma cell lines through Notch signaling显示文摘 | Suwanjunee S Wongchana W Palaga T | 2008 | Anticancer Drugs2008，19，5： | 1 |
| 15 | Notch signaling is activated by TLR stimulation and regulates macrophagefunctions显示文摘 | Palaga T Buranaruk C Rengpipat S | | 0，，01： | 1 |
| 16 | Inhibition of gamma-secretase affects proliferation of leukemia and hepatoma cell lines through Notch signaling显示文摘 | Suwanjunee S Wongchana W Palaga T | | 0，，05： | 1 |
| 17 | A fast and effective dependency graph kernel for PPI relation extraction显示文摘 | Tikk D Palaga P Leser U | 2010 | BMC Bioinformatics2010，11，5： | 1 |
| 18 | TCR-mediated Notch signaling regulates proliferation and IFN-γ production in peripheral T cells显示文摘 | Palaga T Miele L Golde TE | 2003 | J Immunol2003，171，6： | 1 |
| 19 | TCR - mediated Notch signaling regulates proliferation and IFN - gamma production in peripheral T cells显示文摘 | Palaga T Miele L Golde TE | 2003 | J lmmunol2003，171，6： | 1 |
| 20 | Inhibition ofgamma-secretase affects proliferation of leukemia and hepatomacell lines through Notch signaling显示文摘 | Suwanjunee S Wongchana W Palaga T | 2008 | Anticancer Drugs2008，19，5： | 1 |
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