About: Regulating STING in health and disease

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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	Regulating STING in health and disease
Creator	Li, Yang Wilson, Heather Kiss-Toth, Endre
source	Medline; PMC
abstract	The presence of cytosolic double-stranded DNA molecules can trigger multiple innate immune signalling pathways which converge on the activation of an ER-resident innate immune adaptor named “STimulator of INterferon Genes (STING)”. STING has been found to mediate type I interferon response downstream of cyclic dinucleotides and a number of DNA and RNA inducing signalling pathway. In addition to its physiological function, a rapidly increasing body of literature highlights the role for STING in human disease where variants of the STING proteins, as well as dysregulated STING signalling, have been implicated in a number of inflammatory diseases. This review will summarise the recent structural and functional findings of STING, and discuss how STING research has promoted the development of novel therapeutic approaches and experimental tools to improve treatment of tumour and autoimmune diseases.
has issue date	2017-06-07(xsd:dateTime)
bibo:doi	10.1186/s12950-017-0159-2
bibo:pmid	28596706
has license	cc-by
sha1sum (hex)	42106f55a4f8908a520377e4dfa89f96b42e2063
schema:url	https://doi.org/10.1186/s12950-017-0159-2
resource representing a document's title	Regulating STING in health and disease
has PubMed Central identifier	PMC5463399
has PubMed identifier	28596706
schema:publication	J Inflamm (Lond)
resource representing a document's body	covid:42106f55a4f8908a520377e4dfa89f96b42e2063#body_text
is schema:about of	named entity 'inflammatory diseases' named entity 'The presence' named entity 'STING' named entity 'therapeutic' named entity 'STING' named entity 'experimental' named entity 'number' named entity 'activation' named entity 'RNA' named entity 'DNA' named entity 'proteins' named entity 'innate immune' named entity 'STING' named entity 'STimulator of INterferon Genes' named entity 'therapeutic approaches' named entity 'STING' named entity 'human disease' named entity 'autoimmune diseases' named entity 'improve' named entity 'ERIS' named entity 'cell death' named entity 'RNA viruses' named entity 'miR' named entity 'c-di-AMP' named entity 'IRF3' named entity 'dimer' named entity 'early on-set' named entity 'STING' named entity 'monogenic' named entity 'helix' named entity 'lymphocyte' named entity 'lupus' named entity 'tuberculosis Bacteria' named entity 'hydrogen' named entity 'B-form' named entity 'macrophages' named entity 'immunogenic' named entity 'dsDNA virus' named entity 'adaptor protein' named entity 'interferon' named entity 'IFNγ' named entity 'AMP' named entity 'motif' named entity 'negative feedback loop' named entity 'E3 ubiquitin ligase' named entity 'MyD88' named entity 'anti-tumour' named entity 'AMPK' named entity 'nuclear DNA' named entity 'cytotoxic T cells' named entity 'lipid particles' named entity 'inflammatory responses' named entity 'CD8α' named entity 'liposomes' named entity 'molecule' named entity 'lipid biosynthesis' named entity 'liposomes' named entity 'nucleoplasm' named entity 'innate immune' named entity 'cGAS' named entity 'blood vessels' named entity 'interferon' named entity 'negatively regulated' named entity 'STING' named entity 'cGAS' named entity 'STING' named entity 'SLE' named entity 'cholesterol metabolism' named entity 'dimers' named entity 'adenosine deaminase' named entity 'dsDNA' named entity 'RNA' named entity 'Sendai virus' named entity 'RNA' named entity 'type I interferons' named entity 'RNA viruses' named entity 'adenosines' named entity 'STING' named entity 'proinflammatory'

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