Disruption of the c-JUN-JNK Complex by a Cell-permeable Peptide Containing the c-JUN δ Domain Induces Apoptosis and Affects a Distinct Set of Interleukin-1-induced Inflammatory Genes
Open Access
- 1 October 2003
- journal article
- Published by Elsevier in Journal of Biological Chemistry
- Vol. 278 (41), 40213-40223
- https://doi.org/10.1074/jbc.m304058200
Abstract
No abstract availableKeywords
This publication has 40 references indexed in Scilit:
- AP-1 as a regulator of cell life and deathNature Cell Biology, 2002
- AP-1 in cell proliferation and survivalOncogene, 2001
- AP-1 – Introductory remarksOncogene, 2001
- c-Jun N-terminal Kinase Is Essential for Growth of Human T98G Glioblastoma CellsPublished by Elsevier ,2000
- Protein transduction: unrestricted delivery into all cells?Trends in Cell Biology, 2000
- Analysis of the Interaction between c-Jun and c-Jun N-terminal Kinase in VivoJournal of Biological Chemistry, 1998
- Reduced Ubiquitin-Dependent Degradation of c-Jun After Phosphorylation by MAP KinasesScience, 1997
- Pseudo-Prolines as a Solubilizing, Structure-Disrupting Protection Technique in Peptide SynthesisJournal of the American Chemical Society, 1996
- JNK2 contains a specificity-determining region responsible for efficient c-Jun binding and phosphorylation.Genes & Development, 1994
- JNK1: A protein kinase stimulated by UV light and Ha-Ras that binds and phosphorylates the c-Jun activation domainCell, 1994