PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
27716962-6	2016	RESULTS: Continuously produced Ach suppressed IFNalpha-induced STAT1 phosphorylation, but increased the level of a protease, USP18 (both measured by Western blot), which interferes with IFNalpha signaling.	Acetaldehyde	31-34	interferon alpha 1	Homo sapiens	46-54	
27716962-6	2016	RESULTS: Continuously produced Ach suppressed IFNalpha-induced STAT1 phosphorylation, but increased the level of a protease, USP18 (both measured by Western blot), which interferes with IFNalpha signaling.	Acetaldehyde	31-34	interferon alpha 1	Homo sapiens	186-194	
27716962-12	2016	CONCLUSIONS: We conclude that Ach disrupts IFNalpha-induced STAT1 phosphorylation by the up-regulation of USP18 to block the innate immunity protection in HCV-infected liver cells, thereby contributing to HCV-alcohol pathogenesis.	Acetaldehyde	30-33	interferon alpha 1	Homo sapiens	43-51	
26251470-11	2015	We concluded that Ach potentiates the suppressive effects of HCV on activation of ISGs attributable to methylation-dependent dysregulation of IFN-alpha signaling.	Acetaldehyde	18-21	interferon alpha 1	Homo sapiens	142-151