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Sulindac inhibits IKBKB. 12 / 13
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"Consistent with our results, XREF_BIBR have demonstrated that inhibition of IKK2 by sulindac, which is a selective inhibitor of NEMO, resulted in the decrease of IgE stimulated histamine release from mast cells."
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"Concentrations of sulindac that inhibit IKKbeta activity also reduce the proliferation of colon cancer cells."
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"Using a combination of chemical kinase inhibitors and siRNA-mediated knockdown of specific kinases, we found that sulindac inhibits IKKbeta, which, in turn, leads to the p38 MAPK-dependent activation of JNK1."
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"Consistent with our results, xref have demonstrated that inhibition of IKK2 by sulindac, which is a selective inhibitor of NEMO, resulted in the decrease of IgE-stimulated histamine release from mast cells."
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"Aspirin, salicylate, and sulindac can directly bind and inhibit recombinant IKKβ, the upstream positive regulator of NF-κB ( xref )."
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"Moreover, sulindac was reported to inhibit in vitro IKKbeta, but not IKKalpha, protein kinase activity, suggesting that it might be possible to find isoform specific inhibitors of IKK."
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"Consistent with our results, have demonstrated that inhibition of IKK2 by sulindac, which is a selective inhibitor of NEMO, resulted in the decrease of IgE-stimulated histamine release from mast cell[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Consistent with our results, Peng et al. (2005) have demonstrated that inhibition of IKK2 by sulindac, which is a selective inhibitor of NEMO, resulted in the decrease of IgE stimulated histamine rele[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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No evidence text available
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"Sulindac [75], aspirin and salicylate [76] specifically inhibit IkKB kinase activity, and sanguinarine has also been shown to inhibit NFkB activation at the level of IkB phosphorylation [77]."
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"Using a combination of chemical kinase inhibitors and siRNA mediated knockdown of specific kinases, we found that sulindac inhibits IKKbeta, which, in turn, leads to the p38 MAPK dependent activation of JNK1."
19526344
sparser
"Lastly, direct inhibition of IKKβ by aspirin, salicylate, and sulindac may be another mechanism that could account for the antiproliferative effects of these NSAIDs via downregulation of NF-κB-mediated proliferative genes such as interleukin-2 (IL-2), granulocyte-macrophage colony-stimulating factor (GM-CSF), c-myc, cyclin D1, and COX-2, among others."
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