IndraLab

Statements



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"For example NO is known to inhibit NFkB activation."

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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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"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]"

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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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"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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"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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"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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"Treatment with l-NAME increased binding of the NFkappaB subunit p50 to consensus oligonucleotide coated microtiter plates, while having only minimal effect on binding of p65, strongly suggesting that nitric oxide mainly inhibits p50 activation."

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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."