Krüppel‐like factor 15 activates hepatitis B virus gene expression and replication

Jie Zhou, Thomas Tan, Yongjun Tian, Bojian Zheng, J.‐H. James Ou, Eric J. Huang, T.S. Benedict Yen – 18 April 2011 – Hepatitis B virus (HBV) is a small DNA virus that requires cellular transcription factors for the expression of its genes. To understand the molecular mechanisms that regulate HBV gene expression, we conducted a yeast one‐hybrid screen to identify novel cellular transcription factors that may control HBV gene expression. Here, we demonstrate that Krüppel‐like factor 15 (KLF15), a liver‐enriched transcription factor, can robustly activate HBV surface and core promoters.

Hepatic B7 homolog 1 expression is essential for controlling cold ischemia/reperfusion injury after mouse liver transplantation

Shinya Ueki, Antonino Castellaneta, Osamu Yoshida, Kikumi Ozaki, Matthew Zhang, Shoko Kimura, Kumiko Isse, Mark Ross, Lifang Shao, Donna B. Stolz, Angus W. Thomson, Anthony J. Demetris, David A. Geller, Noriko Murase – 18 April 2011 – Ischemia/reperfusion (I/R) injury remains a key risk factor significantly affecting morbidity and mortality after liver transplantation (LT). B7 homolog 1 (B7‐H1), a recently identified member of the B7 family, is known to play important roles in regulating local immune responses.

Efficacy and safety of entecavir versus adefovir in chronic hepatitis B patients with hepatic decompensation: A randomized, open‐label study

Yun‐Fan Liaw, Maria Raptopoulou‐Gigi, Hugo Cheinquer, Shiv Kumar Sarin, Tawesak Tanwandee, Nancy Leung, Cheng‐Yuan Peng, Robert P. Myers, Robert S. Brown, Lennox Jeffers, Naoky Tsai, Jolanta Bialkowska, Shijie Tang, Suzanne Beebe, Elizabeth Cooney – 18 April 2011 – A randomized, open‐label comparative study of entecavir versus adefovir therapy was performed in subjects with chronic hepatitis B who had hepatic decompensation (Child‐Turcotte‐Pugh score ≥7).

Mixed phenotype hepatocellular carcinoma after transarterial chemoembolization and liver transplantation

Chikako Zen, Yoh Zen, Ragai R. Mitry, Denis Corbeil, Jana Karbanová, John O'Grady, John Karani, Pauline Kane, Nigel Heaton, Bernard C. Portmann, Alberto Quaglia – 13 April 2011 – We investigated the phenotype of hepatocellular carcinoma (HCC) in livers removed during transplantation after local ablation therapy by transarterial chemoembolization (TACE).

Epithelial cell specificity and apotope recognition by serum autoantibodies in primary biliary cirrhosis

Guanghua Rong, Renqian Zhong, Ana Lleo, Patrick S.C. Leung, Christopher L. Bowlus, Guo‐Xiang Yang, Chen‐Yen Yang, Ross L. Coppel, Aftab A. Ansari, Dean A. Cuebas, Howard J. Worman, Pietro Invernizzi, Gregory J. Gores, Gary Norman, Xiao‐Song He, M. Eric Gershwin – 12 April 2011 – A major enigma of primary biliary cirrhosis (PBC) is the selective targeting of biliary cells.

Murine hepatic stellate cells veto CD8 T cell activation by a CD54‐dependent mechanism

Frank A. Schildberg, Alexandra Wojtalla, Sören V. Siegmund, Elmar Endl, Linda Diehl, Zeinab Abdullah, Christian Kurts, Percy A. Knolle – 12 April 2011 – The liver has a role in T cell tolerance induction, which is mainly achieved through the functions of tolerogenic hepatic antigen‐presenting cells (APCs) and regulatory T cells. Hepatic stellate cells (HSCs) are known to have various immune functions, which range from immunogenic antigen presentation to the induction of T cell apoptosis. Here we report a novel role for stellate cells in vetoing the priming of naive CD8 T cells.

Serum and liver iron differently regulate the bone morphogenetic protein 6 (BMP6)‐SMAD signaling pathway in mice

Elena Corradini, Delphine Meynard, Qifang Wu, Shan Chen, Paolo Ventura, Antonello Pietrangelo, Jodie L. Babitt – 12 April 2011 – The bone morphogenetic protein 6 (BMP6)‐SMAD signaling pathway is a central regulator of hepcidin expression and systemic iron balance. However, the molecular mechanisms by which iron is sensed to regulate BMP6‐SMAD signaling and hepcidin expression are unknown. Here we examined the effects of circulating and tissue iron on Bmp6‐Smad pathway activation and hepcidin expression in vivo after acute and chronic enteral iron administration in mice.

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