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Science 20 January 1995: Vol. 267. no. 5196, pp. 389 - 393 DOI: 10.1126/science.7824938
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Articles
Science, Vol 267, Issue 5196, 389-393
Copyright © 1995 by American Association for the Advancement of Science
Transcription factor ATF2 regulation by the JNK signal transduction pathway
S Gupta,
D Campbell,
B Derijard,
and
RJ Davis
Department of Biochemistry and Molecular Biology, University of Massachusetts Medical School, Worcester 01605.
Treatment of cells with pro-inflammatory cytokines or ultraviolet radiation causes activation of the c-Jun NH2-terminal protein kinase (JNK). Activating transcription factor-2 (ATF2) was found to be a target of the JNK signal transduction pathway. ATF2 was phosphorylated by JNK on two closely spaced threonine residues within the NH2-terminal activation domain. The replacement of these phosphorylation sites with alanine inhibited the transcriptional activity of ATF2. These mutations also inhibited ATF2-stimulated gene expression mediated by the retinoblastoma (Rb) tumor suppressor and the adenovirus early region 1A (E1A) oncoprotein. Furthermore, expression of dominant-negative JNK inhibited ATF2 transcriptional activity. Together, these data demonstrate a role for the JNK signal transduction pathway in transcriptional responses mediated by ATF2.
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J. Virol.
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- Activation and Interaction of ATF2 with the Coactivator ASC-2 Are Responsive for Granulocytic Differentiation by Retinoic Acid.
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- Defective transcription factor activation for proinflammatory gene expression in poly(ADP-ribose) polymerase 1-deficient glia.
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PNAS
101, 5087-5092
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- Differential regulation of activator protein-1 and heat shock factor-1 in myocardial ischemia and reperfusion injury: role of poly(ADP-ribose) polymerase-1.
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Am J Physiol Heart Circ Physiol
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- RanBPM Is a Phosphoprotein That Associates with the Plasma Membrane and Interacts with the Integrin LFA-1.
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- Transcriptional switch by activating transcription factor 2-derived peptide sensitizes melanoma cells to apoptosis and inhibits their tumorigenicity.
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PNAS
101, 4222-4227
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- Induction of CHOP Expression by Amino Acid Limitation Requires Both ATF4 Expression and ATF2 Phosphorylation.
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- Hypoxia induces differentiation of pulmonary artery adventitial fibroblasts into myofibroblasts.
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Am J Physiol Cell Physiol
286, C416-C425
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- Global Gene Expression Responses of Fission Yeast to Ionizing Radiation.
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Mol. Biol. Cell
15, 851-860
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- Suppression by p38 MAP Kinase Inhibitors (Pyridinyl Imidazole Compounds) of Ah Receptor Target Gene Activation by 2,3,7,8-Tetrachlorodibenzo-p-dioxin and the Possible Mechanism.
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- Calcium- and Proteasome-dependent Degradation of the JNK Scaffold Protein Islet-brain 1.
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- p57KIP2 Modulates Stress-activated Signaling by Inhibiting c-Jun NH2-terminal Kinase/Stress-activated Protein Kinase.
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- Role of the ASK1-SEK1-JNK1-HIPK1 Signal in Daxx Trafficking and ASK1 Oligomerization.
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- Disruption of the c-JUN-JNK Complex by a Cell-permeable Peptide Containing the c-JUN {delta} Domain Induces Apoptosis and Affects a Distinct Set of Interleukin-1-induced Inflammatory Genes.
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- A Peptide Inhibitor of c-Jun N-Terminal Kinase Protects against Both Aminoglycoside and Acoustic Trauma-Induced Auditory Hair Cell Death and Hearing Loss.
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- p38 Kinase Is a Key Signaling Molecule for H-Ras-induced Cell Motility and Invasive Phenotype in Human Breast Epithelial Cells.
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- The effect of RU486 on the gene expression profile in an endometrial explant model.
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- c-Jun N-terminal Kinase Contributes to Apoptotic Synergy Induced by Tumor Necrosis Factor-related Apoptosis-inducing Ligand plus DNA Damage in Chemoresistant, p53 Inactive Mesothelioma Cells.
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- A High-throughput Quantitative Multiplex Kinase Assay for Monitoring Information Flow in Signaling Networks: Application to Sepsis-Apoptosis.
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- Increased Constitutive c-Jun N-terminal Kinase Signaling in Mice Lacking Glutathione S-Transferase Pi.
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- Apoptosis-Signal Regulating Kinase-1 Is Involved in the Low Potassium-Induced Activation of p38 Mitogen-Activated Protein Kinase and c-Jun in Cultured Cerebellar Granule Neurons.
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Brain
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- Recent Advances in the Understanding of Amino Acid Regulation of Gene Expression.
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