       Document 0005
 DOCN  M9620005
 TI    Cupric ion blocks NF kappa B activation through inhibiting the
       signal-induced phosphorylation of I kappa B alpha.
 DT    9602
 AU    Satake H; Suzuki K; Aoki T; Otsuka M; Sugiura Y; Yamamoto T; Inoue J;
       Institute for Chemical Research, Kyoto University, Japan.
 SO    Biochem Biophys Res Commun. 1995 Nov 13;216(2):568-73. Unique Identifier
       : AIDSLINE MED/96063646
 AB    A transcription factor NF kappa B, which regulates expression of various
       cellular genes involved in immune responses and viral genes including
       HIV, is sequestered in the cytoplasm as a complex with an inhibitory
       protein I kappa B. Various extracellular signals induce phosphorylation
       and rapid degradation of I kappa B alpha to release NF kappa B. Cu2+ was
       found to inhibit the activation of NF kappa B induced by TNF-alpha, TPA,
       or H2O2. Deoxycholate treatment of the cytoplasmic extract prepared from
       cells stimulated by TNF-alpha in the presence of Cu2+ resulted in the
       release of NF kappa B from I kappa B alpha, indicating that Cu2+
       interferes with the dissociation of the NF kappa B-I kappa B complex.
       Neither phosphorylation nor degradation of I kappa B alpha was observed
       upon TNF-alpha stimulation in the presence of Cu2+. These results
       indicate that Cu2+ inhibits the release of NF kappa B by blockade of a
       signal leading to the phosphorylation of I kappa B alpha.
 DE    Animal  Base Sequence  Binding Sites  Cell Line  Cell Nucleus/METABOLISM
       Copper/*PHARMACOLOGY  Cytoplasm/METABOLISM  DNA-Binding
       Proteins/*ANTAGONISTS & INHIB  Enhancer Elements (Genetics)  Human
       Hydrogen Peroxide/PHARMACOLOGY  Immunoglobulins, kappa-Chain/GENETICS
       Kinetics  Mice  Molecular Sequence Data  NF-kappa B/ANTAGONISTS &
       INHIB/*METABOLISM  Oligodeoxyribonucleotides  Phosphorylation  Signal
       Transduction/*DRUG EFFECTS  T-Lymphocytes  Tetradecanoylphorbol
       Acetate/PHARMACOLOGY  Tumor Cells, Cultured  Tumor Necrosis
       Factor/PHARMACOLOGY  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

