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Zinc up‐regulates NF‐κB activation via phosphorylation of IκB in HUT‐78 (Th 0 ) cells
Author(s) -
Bao Bin,
Prasad Ananda S.,
Beck Frances W.J.,
Sarkar Fazlul H.
Publication year - 2007
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2007.08.030
Subject(s) - transfection , zinc , phosphorylation , chromosomal translocation , microbiology and biotechnology , nf κb , nfkb1 , transcription factor , biology , chemistry , interleukin 10 , signal transduction , gene , cytokine , immunology , biochemistry , organic chemistry
Nuclear factor of κB (NF‐κB) is a major transcription factor regulating the expression of interleukin‐2 (IL‐2) and interleukin‐2 receptor‐α (IL‐2Rα) in Th 1 cells. We previously demonstrated that zinc increased IL‐2 and IL‐2Rα production via NF‐κB activation in HUT‐78 (Th 0 ) cells. However, the molecular mechanism is not well understood. In this study, we found that zinc increased phosphorylated IκB‐α, NF‐κB translocation and activation, as well as the production of IL‐2 and IL‐2Rα in wild type IκB gene transfected zinc‐sufficient HUT‐78 cells, compared to zinc‐deficient HUT‐78 cells. However, dominant negative IκB gene expression decreased these parameters in zinc‐sufficient cells, suggesting that zinc increased NF‐κB activation via IκB pathway.