FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2008771736> ?p ?o ?g. }

• W2008771736 endingPage "347" @default.
• W2008771736 startingPage "337" @default.
• W2008771736 abstract "Although amphotericin B (AmB) is a major polyene antibiotic against invasive fungal infection, administration to patients sometimes causes inflammatory side effects, which limits the usage of the antibiotic. We studied the intracellular signaling that was induced by AmB. p65 (RelA) of nuclear factor-kappaB (NF-kappaB), a well-known signaling molecule as an inducer of proinflammatory cytokines, was phosphorylated by AmB in RAW264.7 cells, a monocyte-like cell line. Among chemical inhibitors of signaling molecules, U-73122 (phospholipase C (PLC) inhibitor), Gö6976 (protein kinase C (PKC) inhibitor), BAPTA-AM (calcium chelator), LFM-A13 (Bruton's tyrosine kinase (Btk)-specific inhibitor), and PP2 (c-Src kinase inhibitor) suppressed AmB-induced phosphorylation of p65 and translocation of p65 into the nucleus. U-73122 and Gö6976 reduced AmB-mediated induction of proinflammatory cytokines (tumor necrosis factor (TNF)-alpha and interleukin (IL)-6) in RAW264.7 cells. Furthermore, AmB-induced activation of NF-kappaB was observed in toll-like receptor (TLR) 2-expressed cells, and the activation of NF-kappaB was inhibited by U-73122, whereas peptidoglycan-induced NF-kappaB activation, which was also dependent on TLR2, was not inhibited by U-73122. Finally, U-73122 partially suppressed in vivo production of TNF-alpha and IL-6 induced by AmB administration in BALB/c mice. These results suggested that the signaling from AmB stimulation to proinflammatory cytokine production is mediated by TLR2, Btk, PLC, PKC, c-Src and NF-kappaB. These signaling molecules may become a target for chemotherapy suppressing AmB-induced proinflammatory cytokine production." @default.
• W2008771736 created "2016-06-24" @default.
• W2008771736 creator A5007825950 @default.
• W2008771736 creator A5025347618 @default.
• W2008771736 creator A5030535199 @default.
• W2008771736 creator A5036114663 @default.
• W2008771736 creator A5037653983 @default.
• W2008771736 creator A5047709951 @default.
• W2008771736 creator A5050313091 @default.
• W2008771736 creator A5051170470 @default.
• W2008771736 creator A5073916680 @default.
• W2008771736 date "2006-04-01" @default.
• W2008771736 modified "2023-09-23" @default.
• W2008771736 title "Analysis of Amphotericin B-Induced Cell Signaling with Chemical Inhibitors of Signaling Molecules" @default.
• W2008771736 cites W1576671418 @default.
• W2008771736 cites W1982185661 @default.
• W2008771736 cites W1986273292 @default.
• W2008771736 cites W1988502798 @default.
• W2008771736 cites W1988557771 @default.
• W2008771736 cites W2010495686 @default.
• W2008771736 cites W2034371559 @default.
• W2008771736 cites W2043240098 @default.
• W2008771736 cites W2045289795 @default.
• W2008771736 cites W2059211918 @default.
• W2008771736 cites W2069113458 @default.
• W2008771736 cites W2093919412 @default.
• W2008771736 cites W2094557223 @default.
• W2008771736 cites W2100485134 @default.
• W2008771736 cites W2107988027 @default.
• W2008771736 cites W2116424495 @default.
• W2008771736 cites W2120975668 @default.
• W2008771736 cites W2137816745 @default.
• W2008771736 cites W2144474454 @default.
• W2008771736 cites W2148319016 @default.
• W2008771736 cites W2158516918 @default.
• W2008771736 cites W2314302729 @default.
• W2008771736 cites W2385246623 @default.
• W2008771736 cites W4210971654 @default.
• W2008771736 cites W4313347691 @default.
• W2008771736 doi "https://doi.org/10.1111/j.1348-0421.2006.tb03792.x" @default.
• W2008771736 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16625056" @default.
• W2008771736 hasPublicationYear "2006" @default.
• W2008771736 type Work @default.
• W2008771736 sameAs 2008771736 @default.
• W2008771736 citedByCount "18" @default.
• W2008771736 countsByYear W20087717362012 @default.
• W2008771736 countsByYear W20087717362014 @default.
• W2008771736 countsByYear W20087717362017 @default.
• W2008771736 countsByYear W20087717362019 @default.
• W2008771736 crossrefType "journal-article" @default.
• W2008771736 hasAuthorship W2008771736A5007825950 @default.
• W2008771736 hasAuthorship W2008771736A5025347618 @default.
• W2008771736 hasAuthorship W2008771736A5030535199 @default.
• W2008771736 hasAuthorship W2008771736A5036114663 @default.
• W2008771736 hasAuthorship W2008771736A5037653983 @default.
• W2008771736 hasAuthorship W2008771736A5047709951 @default.
• W2008771736 hasAuthorship W2008771736A5050313091 @default.
• W2008771736 hasAuthorship W2008771736A5051170470 @default.
• W2008771736 hasAuthorship W2008771736A5073916680 @default.
• W2008771736 hasConcept C164027704 @default.
• W2008771736 hasConcept C203014093 @default.
• W2008771736 hasConcept C2776070231 @default.
• W2008771736 hasConcept C2776914184 @default.
• W2008771736 hasConcept C2777553839 @default.
• W2008771736 hasConcept C2781236682 @default.
• W2008771736 hasConcept C42362537 @default.
• W2008771736 hasConcept C502942594 @default.
• W2008771736 hasConcept C62478195 @default.
• W2008771736 hasConcept C86803240 @default.
• W2008771736 hasConcept C95444343 @default.
• W2008771736 hasConcept C98274493 @default.
• W2008771736 hasConceptScore W2008771736C164027704 @default.
• W2008771736 hasConceptScore W2008771736C203014093 @default.
• W2008771736 hasConceptScore W2008771736C2776070231 @default.
• W2008771736 hasConceptScore W2008771736C2776914184 @default.
• W2008771736 hasConceptScore W2008771736C2777553839 @default.
• W2008771736 hasConceptScore W2008771736C2781236682 @default.
• W2008771736 hasConceptScore W2008771736C42362537 @default.
• W2008771736 hasConceptScore W2008771736C502942594 @default.
• W2008771736 hasConceptScore W2008771736C62478195 @default.
• W2008771736 hasConceptScore W2008771736C86803240 @default.
• W2008771736 hasConceptScore W2008771736C95444343 @default.
• W2008771736 hasConceptScore W2008771736C98274493 @default.
• W2008771736 hasIssue "4" @default.
• W2008771736 hasLocation W20087717361 @default.
• W2008771736 hasLocation W20087717362 @default.
• W2008771736 hasOpenAccess W2008771736 @default.
• W2008771736 hasPrimaryLocation W20087717361 @default.
• W2008771736 hasRelatedWork W1569382726 @default.
• W2008771736 hasRelatedWork W1652312395 @default.
• W2008771736 hasRelatedWork W1973544072 @default.
• W2008771736 hasRelatedWork W2028667039 @default.
• W2008771736 hasRelatedWork W2056367050 @default.
• W2008771736 hasRelatedWork W2079465807 @default.
• W2008771736 hasRelatedWork W2171065062 @default.
• W2008771736 hasRelatedWork W2331046032 @default.
• W2008771736 hasRelatedWork W2411955162 @default.
• W2008771736 hasRelatedWork W4244477508 @default.

• next