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IL33 — PDCD11
Text-mined interactions from Literome
Matsui et al., Intensive Care Med 2012
:
The production of tumor necrosis factor-alpha ( TNF-a ),
interleukin-10 (IL-10), and NO and the
activation of
NF-?B p65 were reduced by hypothermia, but augmented by hyperthermia at 3-6, 24-48, 48, and 0.5 h, post-treatment initiation, respectively
Choi et al., Biochem Biophys Res Commun 2012
(Inflammation) :
IL-33 induced ICAM-1/VCAM-1 expression was dependent on the regulatory effect of IL-33 on the nuclear factor ( NF ) -?B pathway ;
NF-?B p65 expression was
enhanced by
IL-33 overexpression and, conversely, reduced by IL-33 knockdown
Byun et al., Biochem Biophys Res Commun 2012
(Inflammation) :
In addition, EGCG treated DCs inhibited lipopolysaccharide (LPS) induced production of pro-inflammatory cytokines ( tumor necrosis factor [TNF ] -a,
interleukin [ IL]-1ß, and IL-6 ) and
activation of mitogen activated protein kinases ( MAPKs ), e.g., extracellular signal regulated kinase 1/2 ( ERK1/2 ), p38, c-Jun N-terminal kinase (JNK), and
nuclear factor ?B ( NF-?B ) p65 translocation through 67LR
Demyanets et al., J Mol Cell Cardiol 2013
:
In accordance with the cellular distribution of ST2 receptor, human cardiac fibroblasts and myocytes as well as HCASMC did not respond to treatment with IL-33, as recombinant human
IL-33 did not
induce NF-?B p50 and p65 subunits nuclear translocation or increase IL-6, IL-8, and monocyte chemoattractant protein ( MCP-1 ) level in HACF, HACM and HCASMC
Wilson et al., Nature 1994
:
Interleukin-1 beta converting enzyme ( ICE ) processes an inactive precursor to the proinflammatory cytokine,
interleukin-1 beta, and may
regulate programmed cell death in neuronal cells