About: STAT1 is essential for the inhibition of hepatitis C virus replication by interferon-λ but not by interferon-α

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About: STAT1 is essential for the inhibition of hepatitis C virus replication by interferon-λ but not by interferon-α Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	STAT1 is essential for the inhibition of hepatitis C virus replication by interferon-λ but not by interferon-α
Creator	Hotta, Hak Sada, Kiyonao Chihara, Kazuyasu Honjoh, Chisato Kato, Yuji Takeuchi, Kenji Yamauchi, Shota Yoshiki, Hatsumi
Source	PMC
abstract	Interferon-α (IFN-α) and IFN-λ are structurally distinct cytokines that bind to different receptors, but induce expression of similar sets of genes through Janus kinase (JAK)-signal transducers and activators of transcription (STAT) pathways. The difference between IFN-α and IFN-λ signaling remains poorly understood. Here, using the CRISPR/Cas9 system, we examine the role of STAT1 and STAT2 in the inhibition of hepatitis C virus (HCV) replication by IFN-α and IFN-λ. Treatment with IFN-α increases expression of IFN-stimulated genes (ISGs) such as double-stranded RNA-activated protein kinase (PKR) and decreases viral RNA and protein levels in HCV-infected Huh-7.5 human hepatoma cells. These responses are only partially attenuated by knockout of STAT1 but are abolished by knockout of STAT2. In contrast, the inhibition of HCV replication by IFN-λ is abolished by knockout of STAT1 or STAT2. Microarray analysis reveals that IFN-α but not IFN-λ can induce expression of the majority of ISGs in STAT1 knockout cells. These findings suggest that IFN-α can inhibit HCV replication through a STAT2-dependent but STAT1-independent pathway, whereas IFN-λ induces ISG expression and inhibits HCV replication exclusively through a STAT1- and STAT2-dependent pathway.
has issue date	2016-12-08(xsd:dateTime)
bibo:doi	10.1038/srep38336
bibo:pmid	27929099
has license	cc-by
sha1sum (hex)	f0db5c2d8a3973d7c842d412bbde0642498acd7e
schema:url	https://doi.org/10.1038/srep38336
resource representing a document's title	STAT1 is essential for the inhibition of hepatitis C virus replication by interferon-λ but not by interferon-α
has PubMed Central identifier	PMC5144079
has PubMed identifier	27929099
schema:publication	Sci Rep
resource representing a document's body	covid:f0db5c2d8a3973d7c842d412bbde0642498acd7e#body_text
is schema:about of	named entity 'STAT1' named entity 'independent' named entity 'INDUCE' covid:arg/f0db5c2d8a3973d7c842d412bbde0642498acd7e named entity 'dependent' named entity 'IFN-α' named entity 'induce expression' named entity 'IFN-λ' named entity 'HCV' named entity 'ISG' named entity 'hepatitis C virus' named entity 'STAT1' named entity 'interferon-α' named entity 'IFN' named entity 'infection' named entity 'STAT3' named entity 'STAT1' named entity 'HCV' named entity 'STAT1' named entity 'lentivirus' named entity 'STAT3' named entity 'IFN-λ' named entity 'STAT1' named entity 'STAT1' named entity 'STAT1' named entity 'ISGF3' named entity 'viral RNA' named entity 'IFN-α' named entity 'protein synthesis' named entity 'ISGs' named entity 'IFN' named entity 'HCV' named entity 'phosphorylation' named entity 'STAT1' named entity 'ISG' named entity 'mRNAs' named entity 'supernatants' named entity 'kinetics' named entity 'IFN' named entity 'JAK2' named entity 'amino acids' named entity 'STAT2' named entity 'refractory' named entity 'Immunoblotting' named entity 'IFN' named entity 'IFN' named entity 'Life Technologies' named entity 'Charles M. Rice' named entity 'STAT1' named entity 'viral RNA' named entity 'knockout cells' named entity 'STAT6' named entity 'phosphorylating' named entity 'STAT1' named entity 'STAT1' named entity 'STAT6' named entity 'RNA' named entity 'real-time PCR' named entity 'infection' named entity 'frame shift mutation' named entity 'HCV' named entity 'signal transducers and activators of transcription' named entity 'IRF9' named entity 'STAT2' named entity 'HCV' named entity 'STAT2' named entity 'STAT2' named entity 'IFN-λ' named entity 'plasmid' named entity 'IFNAR' named entity 'STAT1' named entity 'phosphorylation' named entity 'ISGF3' named entity 'STAT1'

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