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BLM — NFKB1

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