About: Viral-Mediated mRNA Degradation for Pathogenesis

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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
has title	Viral-Mediated mRNA Degradation for Pathogenesis
Creator	Liu, Xiaoqing Cai, Qiliang Du, Shujuan
Source	Medline; PMC
abstract	Cellular RNA decay machinery plays a vital role in regulating gene expression by altering the stability of mRNAs in response to external stresses, including viral infection. In the primary infection, viruses often conquer the host cell’s antiviral immune response by controlling the inherently cellular mRNA degradation machinery to facilitate viral gene expression and establish a successful infection. This review summarizes the current knowledge about the diverse strategies of viral-mediated regulatory RNA shutoff for pathogenesis, and particularly sheds a light on the mechanisms that viruses evolve to elude immune surveillance during infection.
has issue date	2018-11-29(xsd:dateTime)
bibo:doi	10.3390/biomedicines6040111
bibo:pmid	30501096
has license	cc-by
sha1sum (hex)	d50946bee04acb73e91b3735ccb661a278b86685
schema:url	https://doi.org/10.3390/biomedicines6040111
resource representing a document's title	Viral-Mediated mRNA Degradation for Pathogenesis
has PubMed Central identifier	PMC6315618
has PubMed identifier	30501096
schema:publication	Biomedicines
resource representing a document's body	covid:d50946bee04acb73e91b3735ccb661a278b86685#body_text
is schema:about of	named entity 'machinery' named entity 'degradation' named entity 'viruses' named entity 'RNA' named entity 'mRNA' named entity 'MEDIATED' named entity 'INCLUDING' named entity 'STRATEGIES' named entity 'REGULATORY RNA' named entity 'RNA DECAY' named entity 'PLAYS' named entity 'MRNA DEGRADATION' named entity 'VIRAL-' named entity 'EVOLVE' named entity 'MRNAS' named entity 'EXTERNAL' named entity 'VITAL' named entity 'MEDIATED' named entity 'ABOUT' named entity 'PRIMARY INFECTION' named entity 'MACHINERY' named entity 'ROLE' named entity 'STABILITY' named entity 'GENE EXPRESSION' named entity 'PATHOGENESIS' named entity 'ALTERING' named entity 'VIRUSES' named entity 'INFECTION' named entity 'HOST CELL' named entity 'VIRAL INFECTION' named entity 'ANTIVIRAL IMMUNE RESPONSE' named entity 'VIRAL GENE EXPRESSION' named entity 'CELLULAR' named entity 'REGULATING' named entity 'ESTABLISH' named entity 'KNOWLEDGE' named entity 'IMMUNE SURVEILLANCE' named entity 'RESPONSE TO' named entity 'LIGHT' named entity 'REVIEW' named entity 'CURRENT' named entity 'PATHOGENESIS' named entity 'STRESSES' named entity 'CONTROLLING' named entity 'DIVERSE' named entity 'SUCCESSFUL' named entity 'MRNA DEGRADATION' named entity '27S' named entity 'MECHANISMS' named entity 'response' named entity 'expression' named entity 'immune response' named entity 'vital' named entity 'viral infection' named entity 'regulating gene expression' named entity 'gene expression' named entity 'infection' named entity 'primary infection' named entity 'host cell's' named entity 'immune response' named entity 'immune surveillance' named entity 'antiviral' named entity 'exoribonuclease' named entity 'deadenylation' named entity 'RNA' named entity 'human T-lymphotropic virus' named entity 'nsP3' named entity 'deadenylation' named entity 'influenza A virus' named entity 'dsRNA' named entity 'protein translation' named entity 'mRNA' named entity 'deadenylation' named entity 'Pol II' named entity 'UPF1' named entity 'RNA-binding proteins' named entity 'deadenylation' named entity 'cytoplasmic' named entity 'RNase'

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