BAY11-7082 and Lactacystein in CD154-induced NF-kappaB activation.
- Author:
Xuan ZHANG
1
;
Wen ZHANG
;
Xiao-feng ZENG
;
Feng-chun ZHANG
;
Fu-lin TANG
;
Meng-xue YU
Author Information
- Publication Type:Journal Article
- MeSH: Acetylcysteine; analogs & derivatives; pharmacology; Apoptosis; drug effects; Burkitt Lymphoma; pathology; CD40 Ligand; pharmacology; Cysteine Proteinase Inhibitors; pharmacology; Enzyme Activation; drug effects; Humans; NF-kappa B; antagonists & inhibitors; metabolism; Nitriles; pharmacology; Sulfones; pharmacology; Tumor Cells, Cultured
- From: Acta Academiae Medicinae Sinicae 2004;26(5):488-491
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the inhibition mechanisms of BAY11-7082 (IkappaB-alpha phosphorylation inhibitor) and Lactacystein (proteosome inhibitor) in CD154-induced NF-kappaB activation.
METHODSWe used recombinant CD154 to stimulate EBV/LMP1 negative Ramos B cell and observed the effects of BAY11-7082 and Lactacystein in CD154-induced NF-kappaB luciferase activation, phosphorylation and degradation of IkappaB-alpha, phosphorylation of p65, and nuclear translocation of NF-kappaB subunits upon CD154 stimulation.
RESULTSBoth BAY11-7082 and Lactacystein abrogated CD154-induced NF-kappaB luciferase activation in Ramos cells. While CD154-induced phosphorylation of p65, phosphorylation and degradation of IkappaB-alpha, and nuclear translocation of p50, p65, and c-Rel were all blocked by BAY11-7082; Lactacystein only inhibited degradation of IkappaB-alpha and p65 nuclear translocation.
CONCLUSIONBAY11-7082 and Lactacystein inhibit CD154-induced NF-kappaB activation through different mechanisms.
