FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2275673931> ?p ?o ?g. }

• W2275673931 endingPage "974" @default.
• W2275673931 startingPage "963" @default.
• W2275673931 abstract "Abstract Development of endotoxin tolerance in macrophages during sepsis reprograms Toll-like receptor 4 signaling to inhibit proinflammatory cytokines without suppressing anti-inflammatory and antimicrobial mediators and protects the host from excessive inflammation and tissue damage. However, endotoxin tolerance renders septic patients immunocompromised and unable to control secondary infections. Although previous studies have revealed the importance of several negative regulators of Toll-like receptor signaling in endotoxin tolerance, the role of Pellino proteins has not been addressed. The present report shows that the induction of endotoxin tolerance in vivo in mice and in vitro in human monocytes and THP-1 and MonoMac-6 macrophages increases the expression of Pellino-3. Overexpression of Pellino-3 in human embryonic kidney 293/Toll-like receptor 2 or 293/Toll-like receptor 4/myeloid differentiation factor-2 cells inhibited Toll-like receptor 2/4-mediated activation of nuclear factor-κB and induction of CXCL-8 mRNA, and Pellino-3 ablation increased these responses. Pellino-3-deficient THP-1 cells had elevated Toll-like receptor 2/4-driven tumor necrosis factor-α, interleukin-6 mRNA, and Toll-like receptor 4-driven CCL5 gene expression in response to Toll-like receptor agonists and heat-killed Escherichia coli and Staphylococcus aureus, cytokines controlled by the MyD88 and Toll-interleukin-1R domain-containing protein inducing interferon-β-mediated pathways, respectively. In addition, deficiency in Pellino-3 slightly increased phagocytosis of heat-killed bacteria. Transfected Pellino-3 inhibited nuclear factor-κB activation driven by overexpression of MyD88, TIR domain-containing adapter inducing interferon-β, interleukin-1R-associated kinase-1, and tumor necrosis factor receptor activator of nuclear factor-κB-binding kinase-1, TGF-β-activated kinase 1, and tumor necrosis factor receptor-associated factor-6, and inhibited interleukin-1R-associated kinase 1 modifications and tumor necrosis factor receptor activator of nuclear factor-κB-binding kinase 1 phosphorylation. Finally, Pellino-3 ablation in THP-1 decreased the extent of endotoxin tolerization. Thus, Pellino-3 is involved in endotoxin tolerance and functions as a negative regulator of Toll-like receptor 2/4 signaling." @default.
• W2275673931 created "2016-06-24" @default.
• W2275673931 creator A5015053116 @default.
• W2275673931 creator A5015698726 @default.
• W2275673931 creator A5049703934 @default.
• W2275673931 creator A5067835602 @default.
• W2275673931 creator A5082514162 @default.
• W2275673931 creator A5086359066 @default.
• W2275673931 date "2015-08-26" @default.
• W2275673931 modified "2023-09-26" @default.
• W2275673931 title "Pellino-3 promotes endotoxin tolerance and acts as a negative regulator of TLR2 and TLR4 signaling" @default.
• W2275673931 cites W1486281956 @default.
• W2275673931 cites W1596708757 @default.
• W2275673931 cites W1834782762 @default.
• W2275673931 cites W1889825709 @default.
• W2275673931 cites W1923060047 @default.
• W2275673931 cites W1926532709 @default.
• W2275673931 cites W1944549670 @default.
• W2275673931 cites W1967404571 @default.
• W2275673931 cites W1968061454 @default.
• W2275673931 cites W1970555242 @default.
• W2275673931 cites W1992517860 @default.
• W2275673931 cites W1993197717 @default.
• W2275673931 cites W1993211211 @default.
• W2275673931 cites W1994942139 @default.
• W2275673931 cites W1994985348 @default.
• W2275673931 cites W1995468432 @default.
• W2275673931 cites W1995586746 @default.
• W2275673931 cites W1995909916 @default.
• W2275673931 cites W2013337875 @default.
• W2275673931 cites W2013601771 @default.
• W2275673931 cites W2013994536 @default.
• W2275673931 cites W2022674935 @default.
• W2275673931 cites W2023002208 @default.
• W2275673931 cites W2026379489 @default.
• W2275673931 cites W2027226645 @default.
• W2275673931 cites W2029547581 @default.
• W2275673931 cites W2034763496 @default.
• W2275673931 cites W2038664197 @default.
• W2275673931 cites W2043638973 @default.
• W2275673931 cites W2043801813 @default.
• W2275673931 cites W2057809738 @default.
• W2275673931 cites W2063214912 @default.
• W2275673931 cites W2064918308 @default.
• W2275673931 cites W2066205838 @default.
• W2275673931 cites W2066299623 @default.
• W2275673931 cites W2068299688 @default.
• W2275673931 cites W2074281999 @default.
• W2275673931 cites W2075141308 @default.
• W2275673931 cites W2082263327 @default.
• W2275673931 cites W2083513831 @default.
• W2275673931 cites W2084231086 @default.
• W2275673931 cites W2085637098 @default.
• W2275673931 cites W2093139840 @default.
• W2275673931 cites W2093598708 @default.
• W2275673931 cites W2097476575 @default.
• W2275673931 cites W2098084836 @default.
• W2275673931 cites W2100326315 @default.
• W2275673931 cites W2107277218 @default.
• W2275673931 cites W2110061191 @default.
• W2275673931 cites W2111428445 @default.
• W2275673931 cites W2113458136 @default.
• W2275673931 cites W2113643327 @default.
• W2275673931 cites W2115195989 @default.
• W2275673931 cites W2118887749 @default.
• W2275673931 cites W2124737195 @default.
• W2275673931 cites W2130884945 @default.
• W2275673931 cites W2132687886 @default.
• W2275673931 cites W2143300196 @default.
• W2275673931 cites W2144704426 @default.
• W2275673931 cites W2149122802 @default.
• W2275673931 cites W2151652295 @default.
• W2275673931 cites W2167059596 @default.
• W2275673931 cites W2169751775 @default.
• W2275673931 cites W2192080449 @default.
• W2275673931 cites W4238234488 @default.
• W2275673931 cites W4248219898 @default.
• W2275673931 doi "https://doi.org/10.1189/jlb.2vma0515-229rr" @default.
• W2275673931 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4661042" @default.
• W2275673931 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26310831" @default.
• W2275673931 hasPublicationYear "2015" @default.
• W2275673931 type Work @default.
• W2275673931 sameAs 2275673931 @default.
• W2275673931 citedByCount "23" @default.
• W2275673931 countsByYear W22756739312016 @default.
• W2275673931 countsByYear W22756739312017 @default.
• W2275673931 countsByYear W22756739312018 @default.
• W2275673931 countsByYear W22756739312020 @default.
• W2275673931 countsByYear W22756739312021 @default.
• W2275673931 countsByYear W22756739312022 @default.
• W2275673931 countsByYear W22756739312023 @default.
• W2275673931 crossrefType "journal-article" @default.
• W2275673931 hasAuthorship W2275673931A5015053116 @default.
• W2275673931 hasAuthorship W2275673931A5015698726 @default.
• W2275673931 hasAuthorship W2275673931A5049703934 @default.
• W2275673931 hasAuthorship W2275673931A5067835602 @default.
• W2275673931 hasAuthorship W2275673931A5082514162 @default.
• W2275673931 hasAuthorship W2275673931A5086359066 @default.

• next