About: JNK and p38 mitogen-activated protein kinase pathways contribute to porcine epidemic diarrhea virus infection

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About: JNK and p38 mitogen-activated protein kinase pathways contribute to porcine epidemic diarrhea virus infection Goto Sponge NotDistinct Permalink

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

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	JNK and p38 mitogen-activated protein kinase pathways contribute to porcine epidemic diarrhea virus infection
Creator	Lee, Changhee Kim, Youngnam Jeon, Ji
Source	Elsevier; Medline; PMC
abstract	Abstract The mitogen-activated protein kinase (MAPK) pathways, which are central building blocks in the intracellular signaling network, are often manipulated by viruses of diverse families to favor their replication. Among the MAPK family, the extracellular signal-regulated kinase (ERK) pathway is known to be modulated during the infection with porcine epidemic diarrhea virus (PEDV); however, involvement of stress-activated protein kinases (SAPKs) comprising p38 MAPK and c-Jun NH2-terminal kinase (JNK) remains to be determined. Therefore, in the present study, we investigated whether activation of p38 MAPK and JNK cascades is required for PEDV replication. Our results showed that PEDV activates p38 MAPK and JNK1/2 up to 24h post-infection, whereas, thereafter their phosphorylation levels recede to baseline levels or even fall below them. Notably, UV-irradiated inactivated PEDV, which can enter cells but cannot replicate inside them, failed to induce phosphorylation of p38 MAPK and JNK1/2 suggesting that viral biosynthesis is essential for activation of these kinases. Treatment of cells with selective p38 or JNK inhibitors markedly impaired PEDV replication in a dose-dependent manner and these antiviral effects were found to be maximal during the early times of the infection. Furthermore, direct pharmacological inhibition of p38 MAPK or JNK1/2 activation resulted in a significant reduction of viral RNA synthesis, viral protein expression, and progeny release. However, independent treatments with either SAPK inhibitor did not inhibit PEDV-induced apoptotic cell death mediated by activation of mitochondrial apoptosis-inducing factor (AIF) suggesting that SAPKs are irrelevant to the apoptosis pathway during PEDV infection. In summary, our data demonstrated critical roles of the p38 and JNK1/2 signaling pathways in facilitating successful viral infection during the post-entry steps of the PEDV life cycle.
has issue date	2016-08-15(xsd:dateTime)
bibo:doi	10.1016/j.virusres.2016.05.018
bibo:pmid	27215486
has license	els-covid
sha1sum (hex)	e3983a3d009096ec06c7b4571447bd3e137ca38c
schema:url	https://doi.org/10.1016/j.virusres.2016.05.018
resource representing a document's title	JNK and p38 mitogen-activated protein kinase pathways contribute to porcine epidemic diarrhea virus infection
has PubMed Central identifier	PMC7114560
has PubMed identifier	27215486
schema:publication	Virus Research
resource representing a document's body	covid:e3983a3d009096ec06c7b4571447bd3e137ca38c#body_text
is schema:about of	named entity 'VIRUS INFECTION' named entity 'apoptosis' named entity 'replication' named entity 'apoptotic cell death' named entity 'kinases' named entity 'enter' named entity 'activates' named entity 'p38' named entity 'levels' named entity 'pharmacological' named entity 'CONTRIBUTE ' named entity 'VIRAL RNA' named entity 'THESE' named entity 'JNK' named entity 'MARKEDLY' named entity 'PATHWAYS' named entity 'STRESS' named entity 'SUCCESSFUL' named entity 'FACTOR' named entity 'IMPAIRED' named entity 'DEMONSTRATED' named entity 'DETERMINED' named entity 'SIGNIFICANT' named entity 'SIGNALING PATHWAYS' named entity 'TREATMENTS' named entity 'UP TO' named entity 'MEDIATED' named entity 'RNA SYNTHESIS' named entity 'INDUCE' named entity 'PHOSPHORYLATION' named entity 'EARLY' named entity 'ANTIVIRAL' named entity 'INHIBITION' named entity 'RELEASE' named entity 'ACTIVATES' named entity 'SUMMARY' named entity 'BASELINE' named entity 'INVOLVEMENT' named entity 'BUILDING' named entity 'INACTIVATED' named entity 'JNK INHIBITORS' named entity 'INDUCED' named entity 'LEVELS' named entity 'INDEPENDENT' named entity 'FACILITATING' named entity 'MODULATED' named entity 'INSIDE' named entity 'REQUIRED' named entity 'PHARMACOLOGICAL' named entity 'VIRAL PROTEIN' named entity 'EITHER' named entity 'PATHWAY' named entity 'TERMINAL' named entity 'DID' named entity 'VIRAL INFECTION' named entity 'IRRADIATED' named entity 'KINASES' named entity 'PRESENT' named entity 'STEPS' named entity 'PORCINE EPIDEMIC DIARRHEA VIRUS' named entity 'POST' named entity 'RESULTS' named entity 'BIOSYNTHESIS' named entity 'EFFECTS' named entity 'ROLES' named entity 'CELLS' named entity 'TIMES' named entity 'LIFE CYCLE' named entity 'MAXIMAL' named entity 'INTRACELLULAR SIGNALING' named entity 'FAMILIES' named entity 'DOSE-DEPENDENT' named entity 'STUDY' named entity 'FAILED' named entity 'CRITICAL' named entity 'BLOCKS' named entity 'FAVOR' named entity 'TREATMENT' named entity 'VIRUSES'

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