Proprotein convertase subtilisin/kexin type 9 (PCSK9): Hepatocyte‐specific low‐density lipoprotein receptor degradation and critical role in mouse liver regeneration

Ahmed Zaid, Anna Roubtsova, Rachid Essalmani, Jadwiga Marcinkiewicz, Ann Chamberland, Josée Hamelin, Michel Tremblay, Hélène Jacques, Weijun Jin, Jean Davignon, Nabil G. Seidah, Annik Prat – 11 April 2008 – The gene encoding the proprotein convertase subtilisin/kexin type 9 (PCSK9) is linked to familial hypercholesterolemia, as are those of the low‐density lipoprotein receptor (LDLR) and apolipoprotein B. PCSK9 enhances LDLR degradation, resulting in low‐density lipoprotein accumulation in plasma.

Visceral fat: A key mediator of steatohepatitis in metabolic liver disease

David van der Poorten, Kerry‐Lee Milner, Jason Hui, Alexander Hodge, Michael I. Trenell, James G. Kench, Roslyn London, Tony Peduto, Donald J. Chisholm, Jacob George – 11 April 2008 – Visceral obesity is intimately associated with metabolic disease and adverse health outcomes. However, a direct association between increasing amounts of visceral fat and end‐organ inflammation and scarring has not been demonstrated.

Requirement of the cyclic adenosine monophosphate response element‐binding protein for hepatitis B virus replication

Bo Kyung Kim, Seoung Ok Lim, Yun Gyu Park – 11 April 2008 – The cyclic adenosine monophosphate–response element (CRE)‐transcription factor complex participates in the regulation of viral gene expression and pathologic processes caused by various viruses. The hepatitis B virus (HBV) enhancer I directs liver‐specific transcription of viral genes and contains a CRE sequence (HBV‐CRE); however, whether the HBV‐CRE and CRE‐binding protein (CREB) are required for the HBV life cycle remains to be determined.

Autophagy in the liver

Xiao‐Ming Yin, Wen‐Xing Ding, Wentao Gao – 7 April 2008 – A great part of our current understanding of mammalian macroautophagy is derived from studies of the liver. The term “autophagy” was introduced by Christian de Duve in part based on ultrastructural changes in rat liver following glucagon injection. Subsequent morphological, biochemical, and kinetics studies of autophagy in the liver defined the basic process of autophagosome formation, maturation, and degradation and the regulation of autophagy by hormones, phosphoinositide 3‐kinases, and mammalian target of rapamycin.

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