About: Suppression of NF-κB Activity: A Viral Immune Evasion Mechanism

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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	Suppression of NF-κB Activity: A Viral Immune Evasion Mechanism
Creator	Zhang, Ling Wu, Ying Cheng, Anchun Wang, Mingshu Chen, Shun Jia, Renyong Chen, Xiaoyue Yang, Qiao Liu, Yunya Yu, Yanling Zhang, Shaqiu Zhao, Xinxin Deng, Liyao Liu, Zhu, Zeng, Id, Dekang Id, Mafeng Id, Qiurui
Source	Medline; PMC
abstract	Nuclear factor-κB (NF-κB) is an important transcription factor that induces the expression of antiviral genes and viral genes. NF-κB activation needs the activation of NF-κB upstream molecules, which include receptors, adaptor proteins, NF-κB (IκB) kinases (IKKs), IκBα, and NF-κB dimer p50/p65. To survive, viruses have evolved the capacity to utilize various strategies that inhibit NF-κB activity, including targeting receptors, adaptor proteins, IKKs, IκBα, and p50/p65. To inhibit NF-κB activation, viruses encode several specific NF-κB inhibitors, including NS3/4, 3C and 3C-like proteases, viral deubiquitinating enzymes (DUBs), phosphodegron-like (PDL) motifs, viral protein phosphatase (PPase)-binding proteins, and small hydrophobic (SH) proteins. Finally, we briefly describe the immune evasion mechanism of human immunodeficiency virus 1 (HIV-1) by inhibiting NF-κB activity in productive and latent infections. This paper reviews a viral mechanism of immune evasion that involves the suppression of NF-κB activation to provide new insights into and references for the control and prevention of viral diseases.
has issue date	2018-08-04(xsd:dateTime)
bibo:doi	10.3390/v10080409
bibo:pmid	30081579
has license	cc-by
sha1sum (hex)	92c932118ed311b25d35527281e7b8568aeb2dcf
schema:url	https://doi.org/10.3390/v10080409
resource representing a document's title	Suppression of NF-κB Activity: A Viral Immune Evasion Mechanism
has PubMed Central identifier	PMC6115930
has PubMed identifier	30081579
schema:publication	Viruses
resource representing a document's body	covid:92c932118ed311b25d35527281e7b8568aeb2dcf#body_text
is schema:about of	named entity 'p65' named entity 'motifs' named entity 'describe' named entity 'proteins' named entity 'kinases' named entity 'p50' named entity 'viruses' named entity 'expression' named entity 'molecules' named entity 'This' named entity 'HIV-1' named entity 'prevention' named entity 'NS3' named entity 'survive' named entity 'proteins' named entity 'viruses' named entity 'strategies' named entity 'transcription factor' named entity 'Suppression' named entity 'IκBα' named entity 'antiviral' named entity 'NF-κB' named entity 'PPase' named entity 'Nuclear factor' named entity 'p65' named entity 'HIV-1' named entity 'viruses' named entity 'NF-κB' named entity 'NS3' named entity 'NF-κB' named entity 'adaptor proteins' named entity 'NF-κB' named entity 'NF-κB' named entity 'human immunodeficiency virus 1' named entity 'Viral' named entity 'coactivators' named entity 'protease' named entity 'HSV-1' named entity 'SUMOylation' named entity 'sterically hinders' named entity 'signaling pathway' named entity 'NF-κB' named entity 'MyD88' named entity 'signaling pathway' named entity 'tripartite motif' named entity 'NF-κB' named entity 'MyD88' named entity 'proteasome' named entity 'protein' named entity 'TRIF' named entity 'RIG-I' named entity 'MuV' named entity 'Us3' named entity 'innate immunity' named entity 'HIV-1' named entity 'antiviral' named entity 'NF-κB' named entity 'NSP5' named entity 'latent infections' named entity 'CD4' named entity 'IκBα' named entity 'memory T cells' named entity 'nucleus'

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