[BAY11-7082 and Lactacystein in CD154-induced NF-kappaB activation].
OBJECTIVE
To investigate the inhibition mechanisms of BAY11-7082 (IkappaB-alpha phosphorylation inhibitor) and Lactacystein (proteosome inhibitor) in CD154-induced NF-kappaB activation.


METHODS
We 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.


RESULTS
Both 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.


CONCLUSIONS
BAY11-7082 and Lactacystein inhibit CD154-induced NF-kappaB activation through different mechanisms.
Zhang
Xuan
X
Department of Rheumatology, PUMC Hospital, CAMS and PUMC, Beijing 100730, China. zxpumch2003@yahoo.com.cn
Zhang
Wen
W
Zeng
Xiao-feng
XF
Zhang
Feng-chun
FC
Tang
Fu-lin
FL
Yu
Meng-xue
MX
D000111:Acetylcysteine / Q000031:analogs & derivatives* / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D002051:Burkitt Lymphoma / Q000473:pathology; D023201:CD40 Ligand / Q000494:pharmacology*; D015853:Cysteine Proteinase Inhibitors / Q000494:pharmacology; D004789:Enzyme Activation / Q000187:drug effects; D006801:Humans; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000378:metabolism*; D009570:Nitriles / Q000494:pharmacology*; D013450:Sulfones / Q000494:pharmacology*; D014407:Tumor Cells, Cultured
C434003:3-(4-methylphenylsulfonyl)-2-propenenitrile; D015853:Cysteine Proteinase Inhibitors; D016328:NF-kappa B; D009570:Nitriles; D013450:Sulfones; C067713:lactacystin; D023201:CD40 Ligand; D000111:Acetylcysteine