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120篇 您的检索式:作者名="Tanapat"
    题名 作者 年代 出处 被引量
1Direct 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 2012Cellular & Molecular Immunology2012,9,2:15
2Increased 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 2016World Journal of Gastroenterology2016,22,37:11
3Notch signaling regulates expression of Mcl-1 andapoptosis in PPD-treated macrophages显示文摘巨噬细胞是为由细菌和病毒的感染的细胞的目标。感染的巨噬细胞的命运在决定主人免疫者反应的结果起一个关键作用。巨噬细胞的 Apoptotic 房间死亡被认为是消除病原体的保护的主人防卫并且感染房间。在这研究,我们调查了槽口在在与结核菌素对待的巨噬细胞调整 apoptosis 发信号的参与净化的蛋白质衍生物(PPD ) 。导出髓的巨噬细胞(BMM ) 与 PPD 对待或与 Mycobacterium bovis 杆菌 Calmette-Gué 感染了的鼠科的骨头; rin (BCG ) 导致了 Notch1 的 upregulation。这 upregulation 在 transcriptional 和翻译层次两个都与 anti-apoptotic 基因 mcl-1 的 upregulation 相关很好。Notch1 和 Mcl-1 的减少的层次在当一个 gamma secretase 禁止者(GSI ) 禁止处理槽口受体,被使用时,与 PPD 对待的 BMM 被观察。而且,在像巨噬细胞的房间线 RAW264.7 的 silencing Notch1 减少了 Mcl-1 蛋白质表示,建议那 Notch1 为在巨噬细胞的 Mcl-1 表示是批评的。apoptotic 房间的重要增加与车辆控制相比面对 GSI 与 PPD 在 BMM 的处理之上被观察对待的房间。最后,在人和老鼠的 mcl-1 倡导者的分析揭示了保存潜在的 CSL/RBP-Jκ有约束力的地点。与 mcl-1 倡导者一起的 Notch1 的协会被染色质 immunoprecipitation 证实。一起拿,这些结果显示 Notch1 禁止直接控制 mcl-1 倡导者与 PPD 刺激的巨噬细胞的 apoptosis。Tanapat P alaga Siriluk Ratanabunyong Thitiporn Pattarakankul Naunpun Sangphech Wipawee Wongchana Yukihiro Hadae Patipark Kueanjinda 2013Cellular & Molecular Immunology2013,10,5:4
4Delta-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 2018World Journal of Gastroenterology2018,24,34:3
5Sex differencesin dendritic atrophy of CA3 pyramidal neurons inresponse to chronic restraint stress显示文摘Galea LA McEwen BS Tanapat P 1997Neuroscience1997,81,:1
6Stress inhibits the proliferation of granule cell precursors in the developing dentate gyrus显示文摘 Galea Liisa AM Gould E 1998Int J Dev Neurosci1998,16,34:1
7Estrogen stimulates a transient increase in the number of new neurons in the dentate gyrus of the adult female rats显示文摘Tanapat P Nicholas B Hastings NB 1999J Neurosci1999,19,:1
8Learning enhances adult neurogenesis in the hippocampal formation 显示文摘Gould E Beylin A Tanapat P 1999Nat Neurosci1999,2,12:1
9Adrenal steroids and N-methyl-D-aspartate receptor activation regulate neurogenesis in the dentate gyrus of adult rats through a common pathway显示文摘Cameron HA Tanapat P Gould E 1998Neuroscience1998,82,2:1
10Lesion-induced proliferation of neuronal progenitors in the dentate gyrus of the adult rat显示文摘Gould E Tanapat P 1997Neuroscience1997,80,2:1
11Neurogenesis in the dentate gyrus of the adult tree shrew is regulated by psychosocial stress and NMDA receptor activation显示文摘 McEwen BS Tanapat P 1997J Neurosci1997,17,9:1
12Learning enhances adult neurogenesis in the adult hippocampal formation显示文摘Gouhl E Beylin A Tanapat P el al 1999Nat Neurosci1999,2,3:1
13Neurogenesis in adulthood: A possible role in learning 显示文摘Gould E Tanapat P Hastings NB 1999Trends Cogn Sci1999,3,:1
14Learning enhances adult neurgenesis in the hippocampal formation显示文摘 Beylin A Tanapat P 1999Nat Neurosci1999,2,:1
15Lesion-induced proliferation of neuronal progenitors in the dentate gyrus of adult rat 显示文摘Gould E Tanapat P 1997Neurosci1997,80,:1
16Sex diffe rences in dendritic atrophy of CA3 pyramidal neurons in response to chronic restraint stress 显示文摘Galea L A M McEwen B S Tanapat P 1997Neurosci1997,81,3:1
17Neurogenesis in thedentate gyrus of the adult tree shrew is regulated bypsychosocial stress and NMDA receptor activation 显示文摘Gould E McEwen BS Tanapat P 1997JNeurosci1997,17,7:1
18Estrogen stimulates a transient increase in the number of new neurons in the dentate gyms of the adult female rat 显示文摘Tanapat P Nicholas B Hastings NB 1999Neuro Sci1999,19,14:1
19Regulation of hippocampal neurogenesis in adulthood 显示文摘Gould E Tanapat P Rydel T 2000Biol Psychiatry2000,48,:1
20Modeling waste manage- ment options for greenhouse gas reduction显示文摘S THOMPSON S TANAPAT 2005Journal of Environmental Informatics2005,6,1:1
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