|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | TGF-β1基因多态性与肝炎后肝纤维化的相关性研究显示文摘目的:探讨TGF-β1基因多态性与肝炎后肝纤维化的关系。方法:以实时荧光PCR结合熔点曲线分析,建立可高通量检测TGF-β1编码区3个单核苷酸多态性(SNPs)位点的LightCycler方法,这3个位点分别为Leu10Pro(T>C)、Arg25Pro(G>C)、Thr263Ile(C>T),并对亚洲人群中HBV感染导致的肝纤维化患者(90例)及高加索人群中HCV感染导致的肝纤维化患者(210例)进行SNP分析,并分别与104例亚洲人群和50例高加索人群正常献血员进行比较。结果:亚洲人群中病患组与正常对照组TGF-β1编码区第25、263位氨基酸皆无基因多态性,与高加索人群的检测结果有显著差异;而亚洲人群第10位氨基酸基因多态性出现频率相对较高,病患组(T/C=0.444/0.556)较正常对照组(T/C=0.514/0.486)突变频率稍高,但无显著差异。在高加索人群HCV感染导致的肝纤维化患者中第10、25位氨基酸基因多态性出现的频率与肝纤维化发展程度(average METAVIR-Score)密切相关。结论:提示TGF-β1基因多态性与高加索人群肝炎后肝纤维化的发生具有重要相关性;与亚洲人群肝炎后肝纤维化发生的相关性有待进一步研究。 | 王皓 杨再兴 高春芳 万漠彬 王晓今 Senait Mengsteab Axel M.Gressner Ralf Weiskirchen | 2004 | 第二军医大学学报2004，25，12： | 5 |
| 2 | Human intestinal acyl-CoA synthetase 5 is sensitive to the inhibitor triacsin C显示文摘AIM:To investigate whether human acyl-CoA synthetase 5(ACSL5) is sensitive to the ACSL inhibitor triacsin C.METHODS:The ACSL isoforms ACSL1 and ACSL5 from rat as well as human ACSL5 were cloned and recombinantly expressed as 6xHis-tagged enzymes.Ni 2+-affinity purified recombinant enzymes were assayed at pH 7.5 or pH 9.5 in the presence or absence of triacsin C.In addition,ACSL5 transfected CaCo2 cells and intestinal human mucosa were monitored.ACSL5 expression in cellular systems was verified using Western blot and immunofluorescence.The ACSL assay mix included TrisHCl(pH 7.4),ATP,CoA,EDTA,DTT,MgCl 2,[9,103 H] palmitic acid,and triton X-100.The 200 μL reaction was initiated with the addition of solubilized,purified recombinant proteins or cellular lysates.Reactions were terminated after 10,30 or 60 min of incubation with Doles medium.RESULTS:Expression of soluble recombinant ACSL proteins was found after incubation with isopropyl betaD-1-thiogalactopyranoside and after ultracentrifugation these were further purified to near homogeneity with Ni 2+-affinity chromatography.Triacsin C selectively and strongly inhibited recombinant human ACSL5 protein at pH 7.5 and pH 9.5,as well as recombinant rat ACSL1(sensitive control),but not recombinant rat ACSL5(insensitive control).The IC50 for human ACSL5 was about 10 μmol/L.The inhibitory triacsin C effect was similar for different incubation times(10,30 and 60 min) and was not modified by the N-or C-terminal location of the 6xHis-tag.In order to evaluate ACSL5 sensitivity to triacsin C in a cellular environment,stable human ACSL5 CaCo2 transfectants and mechanically dissected normal human intestinal mucosa with high physiological expression of ACSL5 were analyzed.In both models,ACSL5 peak activity was found at pH 7.5 and pH 9.5,corresponding to the properties of recombinant human ACSL5 protein.In the presence of triacsin C(25 μmol/L),total ACSL activity was dramatically diminished in human ACSL5 transfectants as well as in ACSL5-rich human intestinal mucosa.CONCLUSION:The data strongly indicate that human ACSL5 is sensitive to triacsin C and does not compensate for other triacsin C-sensitive ACSL isoforms. | Elke Kaemmerer Anne Peuscher Andrea Reinartz Christian Liedtke Ralf Weiskirchen Jürgen Kopitz Nikolaus Gassler | 2011 | World Journal of Gastroenterology2011，17，44： | 3 |
| 3 | The use of marine-derived bioactive compounds as potential hepatoprotective agents显示文摘海洋的环境可以为新奇的药作为富有的来源被探索。很多导出水兵的混合物被孤立并且识别,并且他们的治疗学的效果和药理学侧面被描绘。在现在的评论,我们为肝 fibrotic 疾病的治疗作为潜在的 hepatoprotective 代理人用海洋的混合物加亮最近的研究并且讨论他们的活动的建议机制。另外,在富有的海洋的生活为新奇天赋的隔离提供一个潜力的地方,我们在阿曼讨论类似的研究的意义,在肝疾病上显示治疗学的效果的 bioactive 产品。 | Dileep G NAIR Ralf WEISKIRCHEN Salma K AI-MUSHARAFI | 2015 | Acta Pharmacologica Sinica2015，36，2： | 3 |
| 4 | Endoglin in liver fibrogenesis: Bridging basic science and clinical practice显示文摘Endoglin, also known as cluster of differentiation CD105, was originally identified 25 years ago as a novel marker of endothelial cells. Later it was shown that endoglin is also expressed in pro-fibrogenic cells including mesangial cells, cardiac and scleroderma fibroblasts, and hepatic stellate cells. It is an integral membranebound disulfide-linked 180 kDa homodimeric receptor that acts as a transforming growth factor-β(TGF-β) auxiliary co-receptor. In humans, several hundreds of mutations of the endoglin gene are known that give rise to an autosomal dominant bleeding disorder that is characterized by localized angiodysplasia and arteriovenous malformation. This disease is termed hereditary hemorrhagic telangiectasia type Ⅰ and induces various vascular lesions, mainly on the face, lips, hands and gastrointestinal mucosa. Two variants of endoglin(i.e., S- and L-endoglin) are formed by alternative splicing that distinguishes from each other in the length of their cytoplasmic tails. Moreover, a soluble form of endoglin, i.e.,sol-Eng, is shedded by the matrix metalloprotease-14 that cleaves within the extracellular juxtamembrane region. Endoglin interacts with the TGF-β signaling receptors and influences Smad-dependent and-independent effects. Recent work has demonstrated that endoglin is a crucial mediator during liver fibrogenesis that critically controls the activity of the different Smad branches. In the present review, we summarize the present knowledge of endoglin expression and function, its involvement in fibrogenic Smad signaling, current models to investigate endoglin function, and the diagnostic value of endoglin in liver disease. | Steffen K Meurer Muhammad Alsamman David Scholten Ralf Weiskirchen | 2014 | World Journal of Biological Chemistry2014，5，2： | 3 |
| 5 | Interleukin-33 in the pathogenesis of liver fibrosis: alarming ILC2 and hepatic stellate cells显示文摘 | Ralf Weiskirchen Frank Tacke | 2017 | Cellular & Molecular Immunology2017，14，2： | 3 |
| 6 | Lipid-induced up-regulation of human acyl-CoA synthetase 5 promotes hepatocellular apoptosis显示文摘 | Andrea Reinartz Josef Ehling Andrea Leue Christian Liedtke Ursula Schneider Jürgen Kopitz Thomas Weiss Claus Hellerbrand Ralf Weiskirchen Ruth Knüchel Nikolaus Gassler | 2010 | BBA - Molecular and Cell Biology of Lipids2010，，9： | 2 |
| 7 | Variable expression of cystatin C in cultured trans-differentiating rat hepatic stellate cells显示文摘瞄准:学习 C (CysC ) ,它由转变生长 factor-beta1 (TGF-beta1 ) 的规定和导出血小板的生长因素(PDGF ) 和有在这个特殊房间发信号的 TGF-beta1 的 CysC 的潜在的干扰打的 cystatin 的表示。方法:我们计算了 CysC 表达式在有教养, profibrogenic 肝的星形细胞和区分 trans 的 myofibroblasts 由北、西方弄污并且共焦的激光扫描显微镜学。结果:CysC 在 trans 区别期间显著地被增加。TGF-beta1 和 PDGF-BB 压制了 CysC 表示。而且, CysC 分泌物被处理与 TGF-beta1 导致。尽管 CysC 导致了 TGF 贝它的一种增加的有约束力的亲密关系,受体是由化学 cross-linking 估计了与打 III (beta-glycan )[125I ] 它没调制的 -TGF-beta1, 由评估 Smad2/3 磷酸化地位出现的 TGF-beta1 信号转导变异并且[CAGA ]-MLP-luciferase 记者基因试金。有趣地,流类型 III TGF 贝它受体 beta-glycan 在对待 CysC 的房间被减少。我们的数据显示那 CysC 表情起来在 trans 区别期间调整了。结论:在患肝疾病的病人的浆液的增加的 CysC 层次是至少部分由于在激活的肝的星形细胞的更高的表情。而且, TGF-beta1 影响 CysC 的分泌物,加亮在肝的纤维发生的前进的半胱氨酸朊酶的一个潜在地重要的角色。 | Axel M Gressner Birgit Lahme Steffen K Meurer Olav Gressner Raif Weiskirchen | 2006 | World Journal of Gastroenterology2006，12，5： | 2 |
| 8 | Pro-fibrogenic potential of PDGF-D in liver fibrosis显示文摘 | Erawan Borkham-Kamphorst Claudia R.C. van Roeyen Tammo Ostendorf Jürgen Floege Axel M. Gressner Ralf Weiskirchen | 2007 | Journal of Hepatology2007，，6： | 2 |
| 9 | Roles of TGF-beta in hepatic fibrosis 显示文摘 | Gressner AM Weiskirchen R Breitkopf K | 2002 | Front Biosci2002，7，： | 1 |
| 10 | Modern pathogenetic concepts of liver fibrosis suggest stellate cells and TGF - beta as major players and therapeutic targets显示文摘 | Gressner AM Weiskirchen R | 2006 | J Cell Mol Med2006，10，1： | 1 |
| 11 | Roles of TGF-beta in hepatic fibrosis显示文摘 | Gressner AM Weiskirchen R Breitkopf K | 2002 | Front Biosci2002，7，4： | 1 |
| 12 | LIM-domain proteincysteine-and glycine-rich protein 2(CRP2)is a novel marker ofhepaticstellate cells and binding partner of the protein inhibitor of activatedSTAT1显示文摘 | Weiskirchen R Moser M Weiskirchen S | 2001 | The Biochemical journal2001，359，3： | 1 |
| 13 | Inhibition of hepatic fibrogenesis by matrix metalloproteinase-9 mu- tants in mice显示文摘 | Roderfeld M Weiskirchen R Wagner S | 2006 | FASEB J2006，20，3： | 1 |
| 14 | Cellular and molecular functions of hepatic stellate cells in inflammatory responses and liver immunology显示文摘 | WEISKIRCHEN R TACKE F | 2014 | Hepatobiliary Surg Nutr2014，3，6： | 1 |
| 15 | Modern pathogenetie concepts of liver fibrosis suggest stellate ceils and TGF-beta as major players and therapeutle targets 显示文摘 | Greessner AId Weiskirchen R | 2006 | J Cell Mol Med2006，10，： | 1 |
| 16 | BMP-7 as antagonist of organ fibrosis显示文摘 | Weiskirchen R Meurer SK Gressner OA | 2009 | Front Biosci(Landmark Ed)2009，14，： | 1 |
| 17 | Modem pathogenetic concepts of liver fibrosis suggest stellate cells and TGF-β as major players and therapeutic targets显示文摘 | Gressner AM Weiskirchen R | 2006 | J Cell Mol Med2006，10，1： | 1 |
| 18 | Comparative evaluation of gene delivery devices in primary cultures of rat hepatic stellate cells and rat myofibroblasts 显示文摘 | WEISKIRCHEN R KNEIFEL J WEISKIRCHEN S | 2000 | BMC Cell Biol2000，1，： | 1 |
| 19 | Biomarkers of liver fibrosis: clinical translation o{ molecular pathogenesis or based on liver-dependent malfunction tests 显示文摘 | Gressner OA Weiskirchen R Gressner AM | 2007 | Clin Chim Acta2007，381，2： | 1 |
| 20 | Modern pathogenetic con- cepts of liver fibrosis suggest stellate cells and TGF-beta as major players and therapeutic targets显示文摘 | Gressner AM Weiskirchen R | 2006 | J Cell Mol Med2006，10，1： | 1 |
您所在的机构暂未开通此部分的功能，请联系管理员