FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2913235038> ?p ?o ?g. }

• W2913235038 abstract "TLR4 activation initiates a signaling cascade leading to the production of type I IFNs and of the downstream IFN-stimulated genes (ISGs). Recently, a number of IFN-induced long non-coding RNAs (lncRNAs) that feed-back regulate the IFN response have been identified. Dysregulation of this process, collectively known as the Interferon (IFN) Response, represents a common molecular basis in the development of autoimmune and autoinflammatory disorders. Concurrently, alteration of lncRNA profile has been described in several type I IFN-driven autoimmune diseases. In particular, both TLR activation and the upregulation of ISGs in peripheral blood mononuclear cells have been identified as possible contributors to the pathogenesis of systemic sclerosis (SSc), a connective tissue disease characterized by vascular abnormalities, immune activation, and fibrosis. However, hitherto, a potential link between specific lncRNA and the presence of a type I IFN signature remains unclear in SSc. In this study, we identified, by RNA sequencing, a group of lncRNAs related to the IFN and anti-viral response consistently modulated in a type I IFN-dependent manner in human monocytes in response to TLR4 activation by LPS. Remarkably, these lncRNAs were concurrently upregulated in a total of 46 SSc patients in different stages of their disease as compared to 18 healthy controls enrolled in this study. Among these lncRNAs, Negative Regulator of the IFN Response (NRIR) was found significantly upregulated in vivo in SSc monocytes, strongly correlating with the IFN score of SSc patients. Weighted Gene Co-expression Network Analysis showed that NRIR-specific modules, identified in the two datasets, were enriched in type I IFN and viral response biological processes. Protein coding genes common to the two distinct NRIR modules were selected as putative NRIR target genes. Fifteen in silico-predicted NRIR target genes were experimentally validated in NRIR-silenced monocytes. Remarkably, induction of CXCL10 and CXCL11, two IFN-related chemokines associated with SSc pathogenesis, was reduced in NRIR-knockdown monocytes, while their plasmatic level was increased in SSc patients. Collectively, our data show that NRIR affects the expression of ISGs and that dysregulation of NRIR in SSc monocytes may account, at least in part, for the type I IFN signature present in SSc patients." @default.
• W2913235038 created "2019-02-21" @default.
• W2913235038 creator A5008332699 @default.
• W2913235038 creator A5030007102 @default.
• W2913235038 creator A5036953199 @default.
• W2913235038 creator A5040395746 @default.
• W2913235038 creator A5046171667 @default.
• W2913235038 creator A5052778752 @default.
• W2913235038 creator A5065548367 @default.
• W2913235038 creator A5069565176 @default.
• W2913235038 creator A5082655252 @default.
• W2913235038 creator A5085162857 @default.
• W2913235038 date "2019-01-31" @default.
• W2913235038 modified "2023-10-14" @default.
• W2913235038 title "The Long Non-coding RNA NRIR Drives IFN-Response in Monocytes: Implication for Systemic Sclerosis" @default.
• W2913235038 cites W1490395575 @default.
• W2913235038 cites W1522600439 @default.
• W2913235038 cites W1563659068 @default.
• W2913235038 cites W1594879978 @default.
• W2913235038 cites W1964695094 @default.
• W2913235038 cites W1966327575 @default.
• W2913235038 cites W1968218958 @default.
• W2913235038 cites W1969353942 @default.
• W2913235038 cites W1971174320 @default.
• W2913235038 cites W1991977547 @default.
• W2913235038 cites W1999147414 @default.
• W2913235038 cites W1999746344 @default.
• W2913235038 cites W2000177767 @default.
• W2913235038 cites W2004534466 @default.
• W2913235038 cites W2005066398 @default.
• W2913235038 cites W2006232527 @default.
• W2913235038 cites W2027410633 @default.
• W2913235038 cites W2030479443 @default.
• W2913235038 cites W20377036 @default.
• W2913235038 cites W2039764245 @default.
• W2913235038 cites W2054538838 @default.
• W2913235038 cites W2077655287 @default.
• W2913235038 cites W2081374872 @default.
• W2913235038 cites W2082225136 @default.
• W2913235038 cites W2088656967 @default.
• W2913235038 cites W2089255535 @default.
• W2913235038 cites W2092250990 @default.
• W2913235038 cites W2094596462 @default.
• W2913235038 cites W2097065948 @default.
• W2913235038 cites W2099447582 @default.
• W2913235038 cites W2106022265 @default.
• W2913235038 cites W2117322594 @default.
• W2913235038 cites W2119605300 @default.
• W2913235038 cites W2121343862 @default.
• W2913235038 cites W2124649657 @default.
• W2913235038 cites W2125874167 @default.
• W2913235038 cites W2134526812 @default.
• W2913235038 cites W2138845095 @default.
• W2913235038 cites W2145040563 @default.
• W2913235038 cites W2147320974 @default.
• W2913235038 cites W2152562935 @default.
• W2913235038 cites W2156467055 @default.
• W2913235038 cites W2158007484 @default.
• W2913235038 cites W2159675211 @default.
• W2913235038 cites W2179438025 @default.
• W2913235038 cites W2180591043 @default.
• W2913235038 cites W2202022139 @default.
• W2913235038 cites W2289023840 @default.
• W2913235038 cites W2299513640 @default.
• W2913235038 cites W2394768513 @default.
• W2913235038 cites W2482288331 @default.
• W2913235038 cites W2508060872 @default.
• W2913235038 cites W2512739785 @default.
• W2913235038 cites W2562126123 @default.
• W2913235038 cites W2570492803 @default.
• W2913235038 cites W2604342793 @default.
• W2913235038 cites W2610264107 @default.
• W2913235038 cites W2615184377 @default.
• W2913235038 cites W2746060677 @default.
• W2913235038 cites W2752818119 @default.
• W2913235038 cites W2767718374 @default.
• W2913235038 cites W2804542506 @default.
• W2913235038 cites W2840834498 @default.
• W2913235038 cites W2887313077 @default.
• W2913235038 cites W2911875239 @default.
• W2913235038 cites W30116390 @default.
• W2913235038 cites W34360751 @default.
• W2913235038 doi "https://doi.org/10.3389/fimmu.2019.00100" @default.
• W2913235038 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6371048" @default.
• W2913235038 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30804934" @default.
• W2913235038 hasPublicationYear "2019" @default.
• W2913235038 type Work @default.
• W2913235038 sameAs 2913235038 @default.
• W2913235038 citedByCount "52" @default.
• W2913235038 countsByYear W29132350382019 @default.
• W2913235038 countsByYear W29132350382020 @default.
• W2913235038 countsByYear W29132350382021 @default.
• W2913235038 countsByYear W29132350382022 @default.
• W2913235038 countsByYear W29132350382023 @default.
• W2913235038 crossrefType "journal-article" @default.
• W2913235038 hasAuthorship W2913235038A5008332699 @default.
• W2913235038 hasAuthorship W2913235038A5030007102 @default.
• W2913235038 hasAuthorship W2913235038A5036953199 @default.
• W2913235038 hasAuthorship W2913235038A5040395746 @default.
• W2913235038 hasAuthorship W2913235038A5046171667 @default.

• next