About: Activation of toll-like receptor signaling pathways leading to nitric oxide-mediated antiviral responses

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

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	Activation of toll-like receptor signaling pathways leading to nitric oxide-mediated antiviral responses
Creator	Amarasinghe, Aruna Faizal, Mohamed Careem, Abdul Sarjoon, Mohamed
source	PMC
abstract	Toll-like receptors (TLRs), well-characterized pattern-recognizing receptors of the innate arm of the immune system, are vital in detecting pathogen-associated molecular patterns (PAMPs). The TLR-PAMP interaction initiates an intracellular signaling cascade, predominantly culminating in upregulation of antiviral components, including inducible nitric oxide synthase (iNOS). After activation, various TLR pathways can promote iNOS production via the myeloid differentiation primary response-88 (MyD-88) adapter protein. Subsequently, iNOS facilitates production of nitric oxide (NO), a highly reactive and potent antiviral molecule that can inhibit replication of RNA and DNA viruses. Furthermore, NO can diffuse freely across cell membranes and elicit antiviral mechanisms in various ways, including direct and indirect damage to viral genomes. This review emphasizes current knowledge of NO-mediated antiviral responses elicited after activation of TLR signaling pathways.
has issue date	2016-05-27(xsd:dateTime)
bibo:doi	10.1007/s00705-016-2904-x
bibo:pmid	27233799
has license	no-cc
sha1sum (hex)	55897fae99e6ee416e7d77f405f1b55ff9298a1e
schema:url	https://doi.org/10.1007/s00705-016-2904-x
resource representing a document's title	Activation of toll-like receptor signaling pathways leading to nitric oxide-mediated antiviral responses
has PubMed Central identifier	PMC7087267
has PubMed identifier	27233799
schema:publication	Arch Virol
resource representing a document's body	covid:55897fae99e6ee416e7d77f405f1b55ff9298a1e#body_text
is schema:about of	named entity 'production' named entity 'differentiation' named entity 'TLR' named entity 'iNOS' named entity 'IMMUNE SYSTEM' named entity 'CELL MEMBRANES' named entity 'PRODUCTION' named entity 'SIGNALING PATHWAYS' named entity 'KNOWLEDGE' named entity 'ACTIVATION' named entity 'ELICIT' named entity 'PAMP' named entity 'HIGHLY' named entity 'PRIMARY RESPONSE' named entity 'VIRAL' named entity 'VARIOUS' named entity 'ACROSS' named entity 'INDIRECT' named entity 'PATHWAYS' named entity 'MECHANISMS' named entity 'REPLICATION' named entity 'DETECTING' named entity 'UPREGULATION' named entity 'TLR' named entity 'CULMINATING' named entity 'ANTIVIRAL' named entity 'ASSOCIATED' named entity 'ANTIVIRAL' named entity 'ARM' named entity 'LEADING' named entity 'NITRIC OXIDE' named entity 'ACTIVATION' named entity 'REACTIVE' named entity 'VITAL' named entity 'FREELY' named entity 'PATHOGEN' named entity 'DNA VIRUSES' named entity 'INTERACTION' named entity 'PATTERN' named entity 'INOS' named entity 'CHARACTERIZED' named entity 'DIRECT' named entity 'RECEPTORS' named entity 'TOLL-LIKE RECEPTORS' named entity 'RESPONSES' named entity 'INCLUDING' named entity 'GENOMES' named entity 'MYELOID' named entity 'ADAPTER PROTEIN' named entity 'PATTERNS' named entity 'MOLECULE' named entity 'MEDIATED' named entity 'DIFFUSE' named entity 'PROMOTE' named entity 'RESPONSES' named entity 'RNA' named entity 'MOLECULAR' named entity 'DAMAGE' named entity 'REVIEW' named entity 'NITRIC OXIDE' named entity 'CURRENT' named entity 'TOLL-LIKE RECEPTOR SIGNALING' named entity 'SIGNALING PATHWAYS' named entity 'MEDIATED' named entity 'INTRACELLULAR SIGNALING CASCADE' named entity 'DIFFERENTIATION' named entity 'COMPONENTS' named entity 'INDUCIBLE NITRIC OXIDE SYNTHASE' named entity 'promote' named entity 'interaction' named entity 'After' named entity 'antiviral' named entity 'cell membranes' named entity 'potent' named entity 'primary' named entity 'antiviral' named entity 'upregulation' named entity 'TLR'

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