Modulation of α-enolase post-translational modifications by dengue virus: increased secretion of the basic isoforms in infected hepatic cells.
Higa, Luiza M; Curi, Bruno M; Aguiar, Renato S; Cardoso, Cynthia C; De Lorenzi, André G; Sena, Silvia L F; Zingali, Russolina B; Da Poian, Andrea T.
; 9(8): e88314, 2014.
Artigo em Inglês | MEDLINE | ID: mdl-25171719
Moonlighting glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is required for efficient hepatitis C virus and dengue virus infections in human Huh-7.5.1 cells.
Alpha-enolase regulates hepatitis B virus replication through suppression of the interferon signalling pathway.
Inhibition of p38MAPK and CD137 signaling reduce dengue virus-induced TNF-α secretion and apoptosis.
Acute Hepatitis C Virus Infection Induces Consistent Changes in Circulating MicroRNAs That Are Associated with Nonlytic Hepatocyte Release.
Novel antiviral host factor, TNK1, regulates IFN signaling through serine phosphorylation of STAT1.
Combined Analysis of Metabolomes, Proteomes, and Transcriptomes of Hepatitis C Virus-Infected Cells and Liver to Identify Pathways Associated With Disease Development.
Restrictive influence of SAMHD1 on Hepatitis B Virus life cycle.
Hepatitis C virus represses E-cadherin expression via DNA methylation to induce epithelial to mesenchymal transition in human hepatocytes.
Hepatoma polarization limits CD81 and hepatitis C virus dynamics.
Productive hepatitis C virus infection of stem cell-derived hepatocytes reveals a critical transition to viral permissiveness during differentiation.