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BLM — RELA
Text-mined interactions from Literome
Ishii et al., Toxicol Appl Pharmacol 2002
:
These results suggest that
BLM can directly
induce E-selectin expression with an increase in transcription in endothelial cells through activation and nuclear translocation of
NF-kappaB/Rel without mediation of inflammatory cytokines
Ma et al., Toxicol Lett 2009
(Lung Diseases) :
In the present study, we investigated the cytotoxic effect of BLM on cultured human bronchial epithelial cells ( BECs ) and first confirmed that
BLM induced the transcriptional activation of
NF-kappaB signaling in BECs ... GSK3beta is known to be a key downstream target of Akt, and LY294002, the PI3K ( phosphatidylinositol 3-kinase ) /Akt inhibitor, which promoted the dephosphorylation of GSK3beta, significantly attenuated
BLM induced
NF-kappaB activation ... Next, we further observed that constitutively active GSK3beta stabilized the inhibitor of NF-kappaB ( IkappaBalpha ), inhibited p65 nuclear translocation and partially blocked
BLM induced
NF-kappaB activation ... These results suggest that
BLM can
induce the activation of
NF-kappaB signaling in BECs and this process is tightly associated with the phosphorylation status of GSK3beta, implying a possible regulatory mechanism of NF-kappaB signaling in BECs during the toxic lung injury induced by BLM