1. Hepatitis C virus co-opts innate immunity component for lipid droplet formation 
Daniel J. Felmlee, Thomas F. Baumert 
Journal of Hepatology 
Volume 59, Issue 5, Pages (November 2013)
DOI: /j.jhep
Copyright © 2013 European Association for the Study of the Liver Terms and Conditions

2. Fig. 1
HCV co-opts IKK-α to promote HCV assembly. The canonical nuclear factor (NF)-κB pathway involves an NF-κB family member bound to an inhibitor of NF-κB (IκB) that retains the complex in the cytoplasm. Upon IκB phosphorylation from the IκB kinase (IKK) complex, IκB is degraded, liberating NF-κB to translocate to the nucleus and to regulate genes involved in innate immunity [5]. The IKK complex consists of NF-κB essential modifier (NEMO), and IKK catalytic units IKK-α and IKK-β. The 3′ untranslated region (UTR) contains a pathogen-associated molecular pattern (PAMP) that forms a complex with DDX3X, activating IKK-α. Active IKK-α and CREB binding protein (CBP/p300) subsequently bind the promoter and transcriptionally activate sterol response element binding protein 1 (SREBP-1). SREBP-1 transcriptionally drives lipogenic genes resulting in an accumulation of lipid droplets [6]. HCV uses lipid droplets as platforms for assembly [1], and all of the factors involved in this IKK-α mediated pathway are important for the HCV life cycle [3].
Journal of Hepatology  , DOI: ( /j.jhep )
Copyright © 2013 European Association for the Study of the Liver Terms and Conditions