pubmed-article:20610652 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:20610652 | lifeskim:mentions | umls-concept:C0032403 | lld:lifeskim |
pubmed-article:20610652 | lifeskim:mentions | umls-concept:C0079904 | lld:lifeskim |
pubmed-article:20610652 | lifeskim:mentions | umls-concept:C0333117 | lld:lifeskim |
pubmed-article:20610652 | lifeskim:mentions | umls-concept:C1336636 | lld:lifeskim |
pubmed-article:20610652 | lifeskim:mentions | umls-concept:C1420556 | lld:lifeskim |
pubmed-article:20610652 | lifeskim:mentions | umls-concept:C1424530 | lld:lifeskim |
pubmed-article:20610652 | lifeskim:mentions | umls-concept:C1521761 | lld:lifeskim |
pubmed-article:20610652 | lifeskim:mentions | umls-concept:C1948023 | lld:lifeskim |
pubmed-article:20610652 | lifeskim:mentions | umls-concept:C0887840 | lld:lifeskim |
pubmed-article:20610652 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:20610652 | pubmed:dateCreated | 2010-7-27 | lld:pubmed |
pubmed-article:20610652 | pubmed:abstractText | The role of NF-kappaB in the expression of inflammatory genes and its participation in the overall inflammatory process of chronic diseases and acute tissue injury are well established. We and others have demonstrated a critical involvement of poly(ADP-ribose) polymerase (PARP)-1 during inflammation, in part, through its relationship with NF-kappaB. However, the mechanism by which PARP-1 affects NF-kappaB activation has been elusive. In this study, we show that PARP-1 inhibition by gene knockout, knockdown, or pharmacologic blockade prevented p65 NF-kappaB nuclear translocation in smooth muscle cells upon TLR4 stimulation, NF-kappaB DNA-binding activity, and subsequent inducible NO synthase and ICAM-1 expression. Such defects were reversed by reconstitution of PARP-1 expression. PARP-1 was dispensable for LPS-induced IkappaBalpha phosphorylation and subsequent degradation but was required for p65 NF-kappaB phosphorylation. A perinuclear p65 NF-kappaB localization in LPS-treated PARP-1(-/-) cells was associated with an export rather an import defect. Indeed, whereas PARP-1 deficiency did not alter expression of importin alpha3 and importin alpha4 and their cytosolic localization, the cytosolic levels of exportin (Crm)-1 were increased. Crm1 inhibition promoted p65 NF-kappaB nuclear accumulation as well as reversed LPS-induced p65 NF-kappaB phosphorylation and inducible NO synthase and ICAM-1 expression. Interestingly, p65 NF-kappaB poly(ADP-ribosyl)ation decreased its interaction with Crm1 in vitro. Pharmacologic inhibition of PARP-1 increased p65 NF-kappaB-Crm1 interaction in LPS-treated smooth muscle cells. These results suggest that p65 NF-kappaB poly(ADP-ribosyl)ation may be a critical determinant for the interaction with Crm1 and its nuclear retention upon TLR4 stimulation. These results provide novel insights into the mechanism by which PARP-1 promotes NF-kappaB nuclear retention, which ultimately can influence NF-kappaB-dependent gene regulation. | lld:pubmed |
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pubmed-article:20610652 | pubmed:language | eng | lld:pubmed |
pubmed-article:20610652 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20610652 | pubmed:citationSubset | AIM | lld:pubmed |
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pubmed-article:20610652 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:20610652 | pubmed:month | Aug | lld:pubmed |
pubmed-article:20610652 | pubmed:issn | 1550-6606 | lld:pubmed |
pubmed-article:20610652 | pubmed:author | pubmed-author:BoularesA... | lld:pubmed |
pubmed-article:20610652 | pubmed:author | pubmed-author:SuzukiYasuhir... | lld:pubmed |
pubmed-article:20610652 | pubmed:author | pubmed-author:ZerfaouiMoura... | lld:pubmed |
pubmed-article:20610652 | pubmed:author | pubmed-author:KimJong GJG | lld:pubmed |
pubmed-article:20610652 | pubmed:author | pubmed-author:ZAKR LRL | lld:pubmed |
pubmed-article:20610652 | pubmed:author | pubmed-author:HansChetan... | lld:pubmed |
pubmed-article:20610652 | pubmed:author | pubmed-author:KoochekpourSh... | lld:pubmed |
pubmed-article:20610652 | pubmed:author | pubmed-author:KimHogyoungH | lld:pubmed |
pubmed-article:20610652 | pubmed:author | pubmed-author:JuJihangJ | lld:pubmed |
pubmed-article:20610652 | pubmed:author | pubmed-author:NauraAmarjit... | lld:pubmed |
pubmed-article:20610652 | pubmed:author | pubmed-author:Abd... | lld:pubmed |
pubmed-article:20610652 | pubmed:author | pubmed-author:CatlingAndrew... | lld:pubmed |
pubmed-article:20610652 | pubmed:author | pubmed-author:ErramiYoussef... | lld:pubmed |
pubmed-article:20610652 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:20610652 | pubmed:day | 1 | lld:pubmed |
pubmed-article:20610652 | pubmed:volume | 185 | lld:pubmed |
pubmed-article:20610652 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:20610652 | pubmed:authorsComplete | Y | lld:pubmed |