IndraLab

Statements



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"Next, we examined whether mitochondrial ROS and caspase-1 activation are involved in NiCl -induced apoptosis.Cotreatment with NiCl and Mito-TEMPO suppressed the cleavage of caspase-1, -3 and IL-1β (Figure 6C)."

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"This mechanism would likely be strictly regulated since ROS production downstream of many pattern recognition receptors alone is not sufficient to activate the NLRP3 inflammasome itself and conversely, overproduction of ROS inactivates caspase-1 by covalent modification [XREF_BIBR]."

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"Rather, they induced a cellular state inhibitory to both the autoproteolytic and substrate cleavage activities of caspase-1 which was reversed by the reactive oxygen species (ROS) scavenger N-acetyl-cysteine but not by reducing agents or nitric oxide pathway inhibitors."

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"Moreover, UgU elicited mitochondrial superoxide generation in a dose dependent manner, and a specific scavenger of mitochondrial reactive oxygen species (ROS) diminished UgU induced IL-1beta and caspase-1 activation."

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"The generation of reactive oxygen species (ROS) was proposed to be the common step in Nlrp3 activation largely based on the observation that caspase-1 activation is blocked by ROS inhibitors XREF_BIBR, XREF_BIBR, XREF_BIBR."

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"Some of the disagreements over the role of ROS might be explained by mitochondrial DAMPs or the fact that high ROS levels can inhibit caspase-1."

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"This is in agreement with the finding that ROS actually inhibit caspase-1 through reversible oxidation and glutathionylation of two redox sensitive cysteine residues (C 397 and C 362), which is in contrast to an earlier study."

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"Furthermore, ROS was generated by pneumococcal infection and inhibited caspase-1 activation within 4 h of infection."

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"We also found that the ROS scavenger 4-hydroxyTEMPO (4-HT) prevented GB111-NH 2 -induced caspase-1 cleavage and activation (XREF_FIG)."

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"Autophagy of damaged mitochondria limits ROS modulated caspase-1 activation and seems to negatively regulate pyroptosis [XREF_BIBR]."

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"Moreover, overproduction of ROS will impair caspase-1 competence by oxidation and glutathionylation."

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"In addition, we also demonstrated that ChC or 7-Keto-induced caspase-1 activation was blocked by MR redox platform disruption, ROS scavenging, or gene silencing of TXNIP, a ROS dependent binder of NLRP3 (XREF_FIG C)."

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"In addition, caspase-1 is also unexpectedly directly inhibited by some ROS."

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"However, the role of ROS has been challenged XREF_BIBR, XREF_BIBR and the overproduction of ROS has been shown also to inhibit the activation of caspase-1 XREF_BIBR."

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"In addition, caspase-1 is also unexpectedly directly inhibited by some ROS."

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"In support of this, caspase-1 activation by hyperosmotic stress was inhibited by the mitochondrial ROS inhibitor MitoTEMPO, but not by the NADPH oxidase inhibitor apocynin or the xanthine oxidase inhibitor allopurinol (XREF_FIG)."

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"A recent study using pharmacologic ROS inhibitors and small hairpin RNA (shRNA) to knockdown p22 phox in human monocytic cell lines has shown that NOX activity and ROS stimulate rather than inhibit the activation of caspase-1."

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"Autophagy of damaged mitochondria limits ROS modulated caspase-1 activation and seems to negatively regulate pyroptosis [XREF_BIBR]."

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"Although ROS scavengers potently inhibited RIPK3 dependent caspase 1 activity, they had no effects on RIPK3 dependent caspase 8 activation, indicating that RIPK3 regulates caspase 8 mediated pro-IL-1beta processing through a distinct mechanism."

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"ROS inactivates caspase-1 via oxidation xref ."

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"Moreover, increased ROS can also reversibly inactivate caspase-1 by oxidation and glutathionylation, indicating that increased ROS can also downregulate caspase-1 activity [XREF_BIBR]."

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"In particular, Phox generated ROS downregulate caspase 1, thereby keeping the inflammasome in check and limiting antineutrophil cytoplasmic antibody (ANCA)-induced inflammation."

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"XREF_BIBR, XREF_BIBR However, the role of ROS is still unclear since further studies suggest that increased ROS production may actually inhibit caspase-1 activation."

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"Moreover, increased ROS can also reversibly inactivate caspase-1 by oxidation and glutathionylation, indicating that increased ROS can also downregulate caspase-1 activity [ xref ]."

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"In the macrophages of superoxide dismutase (SOD) 1 deficient mice, higher level of ROS inhibits the activation of CASP1 [XREF_BIBR]."

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"Vitamin C and/or irinotecan administration decreased the plasma level of ROS and IL-6 and increased the expression of collagen type I and caspase-1."