About: Differential Regulation of Type I Interferon and Epidermal Growth Factor Pathways by a Human Respirovirus Virulence Factor

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About: Differential Regulation of Type I Interferon and Epidermal Growth Factor Pathways by a Human Respirovirus Virulence Factor 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	Differential Regulation of Type I Interferon and Epidermal Growth Factor Pathways by a Human Respirovirus Virulence Factor
Creator	Caignard, G Jacob, Y Bouraï, M Komarova, A Mourez, T
Source	PMC
abstract	A number of paramyxoviruses are responsible for acute respiratory infections in children, elderly and immuno-compromised individuals, resulting in airway inflammation and exacerbation of chronic diseases like asthma. To understand the molecular pathogenesis of these infections, we searched for cellular targets of the virulence protein C of human parainfluenza virus type 3 (hPIV3-C). We found that hPIV3-C interacts directly through its C-terminal domain with STAT1 and GRB2, whereas C proteins from measles or Nipah viruses failed to do so. Binding to STAT1 explains the previously reported capacity of hPIV3-C to block type I interferon signaling, but the interaction with GRB2 was unexpected. This adaptor protein bridges Epidermal Growth Factor (EGF) receptor to MAPK/ERK pathway, a signaling cascade recently found to be involved in airway inflammatory response. We report that either hPIV3 infection or transient expression of hPIV3-C both increase cellular response to EGF, as assessed by Elk1 transactivation and phosphorylation levels of ERK1/2, 40S ribosomal subunit protein S6 and translation initiation factor 4E (eIF4E). Furthermore, inhibition of MAPK/ERK pathway with U0126 prevented viral protein expression in infected cells. Altogether, our data provide molecular basis to explain the role of hPIV3-C as a virulence factor and determinant of pathogenesis and demonstrate that Paramyxoviridae have evolved a single virulence factor to block type I interferon signaling and to boost simultaneous cellular response to growth factors.
has issue date	2009-09-18(xsd:dateTime)
bibo:doi	10.1371/journal.ppat.1000587
bibo:pmid	19806178
has license	cc-by
sha1sum (hex)	fe2000f280297c40bc53ce95d703a9ca6aac19fd
schema:url	https://doi.org/10.1371/journal.ppat.1000587
resource representing a document's title	Differential Regulation of Type I Interferon and Epidermal Growth Factor Pathways by a Human Respirovirus Virulence Factor
has PubMed Central identifier	PMC2736567
has PubMed identifier	19806178
schema:publication	PLoS Pathog
resource representing a document's body	covid:fe2000f280297c40bc53ce95d703a9ca6aac19fd#body_text
is schema:about of	named entity 'pathogenesis' named entity 'MAPK/ERK pathway' named entity 'molecular' named entity 'paramyxoviruses' named entity 'individuals' named entity 'responsible' named entity 'viruses' named entity 'DIFFERENTIAL' named entity 'EPIDERMAL GROWTH FACTOR' named entity 'HAVE' named entity 'INFECTED' named entity 'MOLECULAR' named entity 'TRANSIENT EXPRESSION' named entity 'INCREASE' named entity 'ASSESSED' named entity 'BUT' named entity 'DOMAIN' named entity 'RECEPTOR' named entity 'INTERFERON SIGNALING' named entity 'INFECTION' named entity 'BRIDGES' named entity 'UNEXPECTED' named entity 'ITS' named entity 'RESULTING IN' named entity 'CHILDREN' named entity 'PATHWAY' named entity 'ADAPTOR PROTEIN' named entity 'INVOLVED' named entity 'TARGETS' named entity 'NUMBER OF' named entity 'EPIDERMAL GROWTH FACTOR' named entity 'PROTEIN C' named entity 'C PROTEINS' named entity 'STAT1' named entity 'MOLECULAR BASIS' named entity 'PARAMYXOVIRIDAE' named entity 'CELLS' named entity 'RECENTLY' named entity 'INHIBITION' named entity 'LIKE' named entity 'EVOLVED' named entity 'CAPACITY' named entity 'TO EXPLAIN' named entity 'THESE' named entity 'CELLULAR' named entity 'U0126' named entity 'TRANSACTIVATION' named entity 'RESPONSIBLE' named entity 'CHRONIC DISEASES' named entity 'INTERACTION' named entity 'SIMULTANEOUS' named entity 'NIPAH VIRUSES' named entity 'CELLULAR RESPONSE' named entity 'ELK1' named entity 'PHOSPHORYLATION' named entity 'UNDERSTAND' named entity 'MEASLES' named entity 'FOUND' named entity 'PROVIDE' named entity 'DATA' named entity 'ACUTE RESPIRATORY INFECTIONS' named entity 'INDIVIDUALS' named entity 'AIRWAY INFLAMMATION' named entity 'MAPK' named entity 'INFLAMMATORY RESPONSE' named entity 'DIRECTLY' named entity 'BLOCK' named entity 'OUR' named entity 'HUMAN PARAINFLUENZA VIRUS TYPE 3' named entity 'ERK1' named entity 'PROTEIN EXPRESSION' named entity 'TYPE I INTERFERON' named entity 'ROLE' named entity 'PATHWAYS' named entity 'HUMAN' named entity 'REPORT' named entity 'VIRULENCE'

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