Control of IκB-α Proteolysis by Site-Specific, Signal-Induced Phosphorylation

Author:

Brown Keith1,Gerstberger Susan1,Carlson Louise1,Franzoso Guido1,Siebenlist Ulrich1

Affiliation:

1. Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-1876.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

Reference19 articles.

1. BEG, A.A., TUMOR-NECROSIS-FACTOR AND INTERLEUKIN-1 LEAD TO PHOSPHORYLATION AND LOSS OF I-KAPPA-B-ALPHA - A MECHANISM FOR NF-KAPPA-B ACTIVATION, MOLECULAR AND CELLULAR BIOLOGY 13: 3301 (1993).

2. BOURS, V, THE ONCOPROTEIN BCL-3 DIRECTLY TRANSACTIVATES THROUGH KAPPA-B MOTIFS VIA ASSOCIATION WITH DNA-BINDING P50B HOMODIMERS, CELL 72: 729 (1993).

3. BOURS, V, A NOVEL MITOGEN-INDUCIBLE GENE-PRODUCT RELATED TO P50/P105-NF-KAPPA-B PARTICIPATES IN TRANSACTIVATION THROUGH A KAPPA-B SITE, MOLECULAR AND CELLULAR BIOLOGY 12: 685 (1992).

4. BRESSLER, P, MUTATIONAL ANALYSIS OF THE P50-SUBUNIT OF NF-KAPPA-B AND INHIBITION OF NF-KAPPA-B ACTIVITY BY TRANSDOMINANT P50 MUTANTS, JOURNAL OF VIROLOGY 67: 288 (1993).

5. BROWN, K, MUTUAL REGULATION OF THE TRANSCRIPTIONAL ACTIVATOR NF-KAPPA-B AND ITS INHIBITOR, I-KAPPA-B-ALPHA, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 90: 2532 (1993).

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