FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2034159685> ?p ?o ?g. }

• W2034159685 endingPage "1971" @default.
• W2034159685 startingPage "1959" @default.
• W2034159685 abstract "Epigenetic silencing of tumor necrosis factor alpha (TNF-alpha) and interleukin 1beta (IL-1beta) transcription occurs in blood leukocytes of animals and humans after the initiation of severe systemic inflammation (SSI). We previously reported that the epigenetic signature requires induction of NF-kappaB factor RelB, which directs histone H3K9 dimethylation, disrupts assembly of transcription activator NF-kappaB p65, and induces a sustained switch from the euchromatin to heterochromatin. Here, we report the novel findings that intracellular high mobility group box 1 protein (HMGB1) and nucleosome linker histone H1 protein are necessary components of endotoxin-mediated silencing of TNF-alpha in THP-1 human promonocytes. HMGB1 binds the TNF-alpha promoter during transcription silencing and promotes assembly of the repressor RelB. Depletion of HMGB1 by small interfering RNA results in dissociation of RelB from the promoter and partially restores TNF-alpha transcription. Histone H1, which typically displaces HMGB1 from nucleosomal DNA, also binds concomitantly with HMGB1 to the heterochromatin of the silenced TNF-alpha promoter. Combined knockdown of HMGB1 and H1 restores binding of the transcriptionally active NF-kappaB p65 and reestablishes TNF-alpha mRNA levels. Chromatin reimmunoprecipitation experiments demonstrate that HMGB1 and H1 are likely recruited to TNF-alpha sequences independently and that their binding correlates with histone H3K9 dimethylation, as inhibition of histone methylation blocks HMGB1 and H1 binding. Moreover, HMGB1- and H1-mediated chromatin modifications are gene specific during endotoxin silencing in that they also bind and repress acute proinflammatory IL-1beta, while no binding nor repression of antiinflammatory IkappaBalpha is observed. Finally, we find that H1 and HMGB1 bind to the TNF-alpha a promoter in human leukocytes obtained from patients with SSI. We conclude proinflammatory HMGB1 and structural nucleosome linker H1 couple as a component of the epigenetic complex that silences acute proinflammatory TNF-alpha during the assembly of heterochromatin in the SSI phenotype." @default.
• W2034159685 created "2016-06-24" @default.
• W2034159685 creator A5009228621 @default.
• W2034159685 creator A5024933730 @default.
• W2034159685 creator A5033126095 @default.
• W2034159685 creator A5047444154 @default.
• W2034159685 creator A5061643459 @default.
• W2034159685 creator A5091070290 @default.
• W2034159685 date "2009-04-01" @default.
• W2034159685 modified "2023-10-16" @default.
• W2034159685 title "Chromatin-Specific Remodeling by HMGB1 and Linker Histone H1 Silences Proinflammatory Genes during Endotoxin Tolerance" @default.
• W2034159685 cites W1491793883 @default.
• W2034159685 cites W1538862365 @default.
• W2034159685 cites W1773515121 @default.
• W2034159685 cites W1967507626 @default.
• W2034159685 cites W1968044233 @default.
• W2034159685 cites W1969826234 @default.
• W2034159685 cites W1969863232 @default.
• W2034159685 cites W1977472645 @default.
• W2034159685 cites W1978660434 @default.
• W2034159685 cites W1988626539 @default.
• W2034159685 cites W1997564374 @default.
• W2034159685 cites W1998355675 @default.
• W2034159685 cites W2001149454 @default.
• W2034159685 cites W2004266769 @default.
• W2034159685 cites W2004681520 @default.
• W2034159685 cites W2017314177 @default.
• W2034159685 cites W2029068688 @default.
• W2034159685 cites W2030278030 @default.
• W2034159685 cites W2032909169 @default.
• W2034159685 cites W2032970638 @default.
• W2034159685 cites W2039820190 @default.
• W2034159685 cites W2041086054 @default.
• W2034159685 cites W2041308303 @default.
• W2034159685 cites W2041787701 @default.
• W2034159685 cites W2042821764 @default.
• W2034159685 cites W2058448711 @default.
• W2034159685 cites W2061163173 @default.
• W2034159685 cites W2062553756 @default.
• W2034159685 cites W2063516501 @default.
• W2034159685 cites W2076143571 @default.
• W2034159685 cites W2084413077 @default.
• W2034159685 cites W2085677283 @default.
• W2034159685 cites W2087328770 @default.
• W2034159685 cites W2097599259 @default.
• W2034159685 cites W2101815785 @default.
• W2034159685 cites W2118750743 @default.
• W2034159685 cites W2125175295 @default.
• W2034159685 cites W2132687886 @default.
• W2034159685 cites W2135374161 @default.
• W2034159685 cites W2139562516 @default.
• W2034159685 cites W2143845633 @default.
• W2034159685 cites W2146807706 @default.
• W2034159685 cites W2155740016 @default.
• W2034159685 cites W2157856503 @default.
• W2034159685 cites W2159416234 @default.
• W2034159685 cites W2160369507 @default.
• W2034159685 cites W2164714222 @default.
• W2034159685 cites W2165002886 @default.
• W2034159685 cites W2167169717 @default.
• W2034159685 cites W2167184573 @default.
• W2034159685 cites W2168268248 @default.
• W2034159685 cites W2168798460 @default.
• W2034159685 cites W2171028311 @default.
• W2034159685 cites W2334459983 @default.
• W2034159685 cites W4238941978 @default.
• W2034159685 cites W73359563 @default.
• W2034159685 doi "https://doi.org/10.1128/mcb.01862-08" @default.
• W2034159685 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2655606" @default.
• W2034159685 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19158276" @default.
• W2034159685 hasPublicationYear "2009" @default.
• W2034159685 type Work @default.
• W2034159685 sameAs 2034159685 @default.
• W2034159685 citedByCount "132" @default.
• W2034159685 countsByYear W20341596852012 @default.
• W2034159685 countsByYear W20341596852013 @default.
• W2034159685 countsByYear W20341596852014 @default.
• W2034159685 countsByYear W20341596852015 @default.
• W2034159685 countsByYear W20341596852016 @default.
• W2034159685 countsByYear W20341596852017 @default.
• W2034159685 countsByYear W20341596852018 @default.
• W2034159685 countsByYear W20341596852019 @default.
• W2034159685 countsByYear W20341596852020 @default.
• W2034159685 countsByYear W20341596852021 @default.
• W2034159685 countsByYear W20341596852022 @default.
• W2034159685 countsByYear W20341596852023 @default.
• W2034159685 crossrefType "journal-article" @default.
• W2034159685 hasAuthorship W2034159685A5009228621 @default.
• W2034159685 hasAuthorship W2034159685A5024933730 @default.
• W2034159685 hasAuthorship W2034159685A5033126095 @default.
• W2034159685 hasAuthorship W2034159685A5047444154 @default.
• W2034159685 hasAuthorship W2034159685A5061643459 @default.
• W2034159685 hasAuthorship W2034159685A5091070290 @default.
• W2034159685 hasBestOaLocation W20341596851 @default.
• W2034159685 hasConcept C101762097 @default.
• W2034159685 hasConcept C103435993 @default.
• W2034159685 hasConcept C104317684 @default.
• W2034159685 hasConcept C119056186 @default.

• next