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您的检索式：作者名="Benedetta Lombardi"
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| 1 | PNPLA3 I148M polymorphism and progressive liver disease显示文摘The 148 Isoleucine to Methionine protein variant(I148M)of patatin-like phospholipase domain-containing 3(PNPLA3),a protein is expressed in the liver and is involved in lipid metabolism,has recently been identified as a major determinant of liver fat content.Several studies confirmed that the I148M variant predisposes towards the full spectrum of liver damage associated with fatty liver:from simple steatosis to steatohepatitis and progressive fibrosis.Furthermore,the I148M variant represents a major determinant of progression of alcohol related steatohepatitis to cirrhosis,and to influence fibrogenesis and related clinical outcomes in chronic hepatitis C virus hepatitis,and possibly chronic hepatitis B virus hepatitis,hereditary hemochromatosis and primary sclerosing cholangitis.All in all,studies suggest that the I148M polymorphism may represent a general modifier of fibrogenesis in liver diseases.Remarkably,the effect of the I148M variant on fibrosis was independent of that on hepatic steatosis and inflammation,suggesting that it may affect both the quantity and quality of hepatic lipids and the biology of non-parenchymal liver cells besides hepatocytes,directly promoting fibrogenesis.Therefore,PNPLA3 is a key player in liver disease progression.Assessment of the I148M polymorphism will possibly inform clinical practice in the future,whereas the determination of the effect of the 148M variant will reveal mechanisms involved in hepatic fibrogenesis. | Paola Dongiovanni Benedetta Donati Roberta Fares Rosa Lombardi Rosellina Margherita Mancina Stefano Romeo Luca Valenti | 2013 | World Journal of Gastroenterology2013，19，41： | 17 |
| 2 | The Arabidopsis COP9 SIGNALOSOME INTERACTING F-BOX KELCH 1 Protein Forms an SCF Ubiquitin Ligase and Regulates Hypocotyl Elongation显示文摘由 ubiquitin proteasome 系统(不间断电源) 的蛋白质周转的规定是在优核质的主要 posttranslational 机制。UPS,的关键部件之一 COP9 signalosome (CSN ) ,调整 cullinring E3 ubiquitin ligases。在植物, CSN 参予多样的细胞、发展的进程,从到房间周期控制的轻发信号。在这个工作,我们孤立新植物特定的交往 CSN F 盒子蛋白质,我们它给 CFK1 (COP9 交往 F 盒子 KELCH 1 ) 取名。我们证明在 Arabidopsis thaliana, CFK1 是功能的 ubiquitin ligase 建筑群的一个部件。我们也证明那 CFK1 稳定性被 CSN 并且由 proteasome 依赖的解朊作用调整,并且那盏灯在胚轴导致 CFK1 抄本的累积。CFK1 的分析击倒,异种,和 overexpressing 幼苗显示 CFK1 由增加支持胚轴延伸房间尺寸。CSN 层次的减小提高弄空 CFK1 的幼苗的短胚轴显型,当 CSN 活动的完全的损失压制 CFK1-overexpressing 幼苗的长胚轴的显型时。我们建议那 CFK1 (并且它由 CSN 的规定) 细胞的机制的一个新奇部件正在控制胚轴延伸。 | Anna Franciosini Benedetta Lombardi Silvia lafrate Valeria.Pecce Giovanni Mele Leonardo Lupacchini Gianmarco Rinaldi Youichi Kondou Giuliana Gusmaroli Shiori Aki Tomohiko Tsuge Xing-Wang Deng Minami Matsui Paola Vittorioso Paolo Costantin Giovanna Serino | 2013 | Molecular Plant2013，6，5： | 3 |
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