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Nitric oxide inhibits NFKB1. 16 / 16
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"As a limitation, other potential underlying mechanisms such as decreased mRNA 43, increased degradation of sGC, or high NO induced NFkB activation that downregulate sGC XREF_BIBR, XREF_BIBR have not been addressed by our study 63 and can not be excluded."
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"Moreover, enhanced NO production can be responsible for decreased TNF production, as NO was described to inhibit NFkB transcription factor involved in synthesis of TNF-alpha and several cytokines (Man[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
10802291
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"Inhibition of NO synthase by l -NAME increased p50 activation in the absence of shear, and prevented the downregulation of p50 activity at 90 min."
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"The reduction in NO production determined by ebselen in RIN cells was associated with a decrease in iNOS mRNA expression but not with an inhibition of IL-1- induced NF-KB activation."
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"We and others have shown that the endogenous mediator nitric oxide (NO) inhibits NF-KB and endothelial cell activation through a non cGMPdependent mechanism, s-ldegrees One of the mechanisms by which NO inhibits NF-KB activation is via the transcriptional induction of IKB-ot.11 '12 The following sections, therefore, describe methods used to study the induction of IKB-a by NO.MethodsGeneral ConsiderationsSeveral methods are useful in assessing the induction of IKB-ot by NO."
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"Recently it has been reported that NO inhibits the activation of the transcription factor NF-KB (21)."
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"For example NO is known to inhibit NFkB activation."
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"Indeed, our group has shown that NO inhibits the activation of NFKB like transcriptional regulatory proteins, which are activated by reactive oxygen species and mediate transcription of numerous genes implicated in the pathogenesis of atherosclerosis.4 These findings pointed towards a molecular link between endothelial NO synthesis and oxidant sensitive transcriptional regulatory mechanisms involved in the protective effects of intact endothelial function."
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"9The ability of NO to inhibit NFKB and TNF ~ may be relevant to vascular disease because TNFo ~ and hypercholesterolemia have both been shown to increase superoxide (02) production in endothelial cellsP8 The conversion of OF to hydrogen peroxide (H202) by the enzyme superoxide dismutase (SOD) may then lead to the modulation of redox sensitive signaling pathwaysincluding Ras, protein kinases (PK) and phosphatases (PPase) (Fig 2)."
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"S-nitrosylation would affect the binding of P50 to DNA, and spermine NONOate, a NO donor, inhibited the organization of P50 and DNA complexes [138] ."
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"Research has demonstrated that NO donors inhibit the production of inflammatory cytokines (TNF-α, IL-1, MIP-1α) and NF-KB activation in lung macrophages."
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"For example, NO 2 -FAs inhibit NFkB activity by nitroalkylating the p65 subunit, thereby suppressing NFkB mediated pro inflammatory cytokine and adhesion protein expression [XREF_BIBR]."
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"In our hands, NO inhibits HIV 1 replication in infected peripheral blood mononuclear cells, suggesting that NO may inhibit NF-KB activity in these cells."
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"miR-369 has emerged as a key regulator of inflammatory response in dendritic cells since it decreases LPS-induced NO production, by directly targeting iNOS expression and simultaneously inhibiting nuclear translocation of NFKB (76)."
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"High NO concentrations after iNOS stimulation inhibit protein adhesion expression on endothelial cells due to S-nitrosylation of p50 and p65 in NF-κB and IKKβ (Aguilar et al., 2020)."
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"We and others have shown that the endogenous mediator nitric oxide (NO) inhibits NF-KB and endothelial cell activation through a non cGMPdependent mechanism, s-ldegrees One of the mechanisms by which NO inhibits NF-KB activation is via the transcriptional induction of IKB-ot.11 '12 The following sections, therefore, describe methods used to study the induction of IKB-a by NO.MethodsGeneral ConsiderationsSeveral methods are useful in assessing the induction of IKB-ot by NO."
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