IndraLab

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Nitric oxide inhibits CASP1. 30 / 30
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"Under these conditions, NO also inhibited IL-1beta secretion and caspase-1 activation but did not affect IL-6 or TNF-alpha secretion (XREF_FIG and XREF_FIG and XREF_SUPPLEMENTARY and XREF_SUPPLEMENTARY), and NLRP3 or ASC expression (XREF_FIG)."
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"Nitric oxide suppresses NLRP3 inflammasome mediated IL-1beta secretion and caspase-1 activation in mouse macrophages."
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"Although NO can inhibit caspase-1 activity by direct modification XREF_BIBR, XREF_BIBR, we asked whether the inhibitory effect of NO on ASC pyroptosome formation was caspase-1 independent."
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"Indeed, Dimmeler et al. [16] have recently shown that caspase-1 and caspase-3 are inhibited by nitric oxide, and they provide evidence for nitrosylation of the active site thiol group."
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"In addition, increased expression of NOS2 in PDE3B -/- adipose tissue may contribute to increased NO (XREF_FIG), which inhibits caspase-1, preventing release of IL1beta and IL18 XREF_BIBR, and inhibit NLRP3 inflammasome activation XREF_BIBR."
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"Since NO inhibits caspase 1 activity, this provides a potential feedback loop, whereby IL-18 may regulate its own cleavage [22,26]."
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"Since NO inhibits caspase 1 activity, this provides a potential feedback loop whereby IL-18 may regulate its own cleavage."
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"Although the reason for such a decrease in IL-18 levels in patients with CM was not clear from the present study, it is possible that nitric oxide (NO), if produced in cases with CM, may suppress the [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Thus, the downregulation of caspase-1 by NO may be important for the negative regulation of IL-18 and -1 beta.Recently, caspase-1-independent secretion of IL-1beta was demonstrated [34]."
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"The NO donor S-nitroso-N-acetyl-DL-penicillamine inhibited caspase-1 activity in cells as well as the activity of purified recombinant caspase-1 and also prevented the cleavage of pro-IL-1beta and pro IGIF by recombinant caspase-1."
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"In this study, we found that NO not only inhibits NLRP3 inflammasome mediated IL-1beta secretion and caspase-1 activation, but also inhibits NLRC4- and AIM-2-mediated IL-1beta secretion and caspase-1 activation (XREF_SUPPLEMENTARY), but to a much less extent (3-fold decrease for NLRC4 and AIM-2, 40-fold decrease for NLRP3)."
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"These data provide clear evidence that NO suppresses NLRP3 inflammasome mediated IL-1beta secretion and caspase-1 activation in mouse macrophages."
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"Recently, it was shown that nitric oxide (NO) can suppress directly the action of caspase-1, resulting in the prevention of IL-1beta and IL-18 secretion [33]."
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"The blockade of CD36 had no effect on PrP 106-126 -stimulated NF-kappaB activation and TNF-alpha protein release, abrogated the PrP 106-126 -induced iNOS stimulation, downregulated IL-1beta and IL-6 expression at both mRNA and protein levels as well as TNF-alpha mRNA expression, decreased NO production and Fyn phosphorylation, reduced caspase-1 cleavage induced by moderate PrP 106-126 -treatment, but had no effect on caspase-1 activation after treatment with a high concentration of PrP 106-126."
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"Recently, it was shown that nitric oxide (NO) can suppress directly the action of caspase-1, resulting in the prevention of IL-1beta and IL-18 secretion [33]."
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"On the other hand , nitric oxide inhibits caspase-1 activity , providing a potential feedback loop whereby IL-18 may regulate its own cleavage , although its indication for treatment of RA remains unclear [ 182 ] ."
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"It was previously shown that inflammasome activation was inversely correlated to iNOS expression, and that NO inhibited IL-1beta production and caspase-1 activation."
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"It has been reported that NO can inhibit caspase-1 activity by direct modification XREF_BIBR, XREF_BIBR."
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"Suppression of Apoptosis by Nitric Oxide via Inhibition of Interleukin-1beta-converting Enzyme (ICE)-like and Cysteine Protease Protein (CPP)-32-like Proteases."
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"These data indicate that the inhibitory effect of NO on NLRP3 mediated ASC pyroptosome formation is completely independent of caspase-1."
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"The findings reported above suggested that exogenous NO donors inhibited NLRP3 inflammasome mediated IL-1beta secretion and caspase-1 activation."
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"Suppression of apoptosis by nitric oxide via inhibition of interleukin-1beta-converting enzyme (ICE)-like and cysteine protease protein (CPP)-32-like proteases."
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"Endogenous NO produced by iNOS negatively regulates NLRP3 inflammasome mediated IL-1beta secretion and caspase-1 activation."
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"As NO has been found to inhibit caspase-1, IL-1beta, and IL-18 release from macrophages, it was suggested that the ability of RLX to promote eNOS induced NO correlated with the RLX induced attenuation of NLRP3 inflammasome induced caspase-1 that was measured in the murine model studied."
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"Similar to what was observed above, NO inhibited IL-1beta secretion and caspase-1 activation under different TLR stimulation conditions (XREF_SUPPLEMENTARY and XREF_SUPPLEMENTARY)."
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"The inhibition of caspase-1 by NO was reversible by the addition of DTT, which is consistent with S nitrosylation as the mechanism of caspase-1 inhibition."
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"In this case, NO also suppressed NLRP3 inflammasome mediated caspase-1 activation (XREF_SUPPLEMENTARY)."
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"A previous study showed that NO could suppress caspase-1 in murine macrophages, resulting in decreased IL-1beta [XREF_BIBR]."
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"NO also suppresses the activity of caspase-1 enzyme which mediates processing of premature IL-1β and IL-18 cytokines, causing decreased IL-1β and IL-18 production [57,58]."
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"Although the reason for such a decrease in IL-18 levels in patients with CM was not clear from the present study, it is possible that nitric oxide (NO), if produced in cases with CM, may suppress the [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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