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M9620005.TXT
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1996-02-26
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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).