Abstract
The transcription activator protein-1 (AP-1) complex is a heterodimer consisting of Fos and Jun family members. We found that extracellular ATP stimulated AP-1 DNA binding activity in cerebral cortical astrocyte cultures. This activity was maximal at 1 h and persisted for at least 3 h post-treatment. Shift-Western blotting indicated the presence of c-Fos in the AP-1 complexes. Stimulation of AP-1 binding by ATP was due to activation of P2 rather than P1 purinoceptors. The protein kinase C (PKC) inhibitor Ro 31-8220 markedly reduced P2 purinoceptor-mediated AP-1 induction. The induction of AP-1 complexes by ATP may contribute to changes in gene expression which underlie the trophic effects of extracellular ATP on astrocytes.
Publication types
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adenosine Triphosphate / pharmacology*
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Animals
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Astrocytes / drug effects
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Astrocytes / metabolism*
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Blotting, Western
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Cell Nucleus / drug effects
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Cell Nucleus / metabolism
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Cells, Cultured
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Cerebral Cortex / cytology
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Cerebral Cortex / drug effects
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Cerebral Cortex / metabolism
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Extracellular Space / drug effects
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Extracellular Space / metabolism
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Glial Fibrillary Acidic Protein / biosynthesis
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Protein Kinase C / antagonists & inhibitors
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Protein Kinase C / metabolism
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Proto-Oncogene Proteins c-fos / biosynthesis
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Rats
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Receptors, Purinergic P2 / drug effects
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Receptors, Purinergic P2 / metabolism*
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Signal Transduction / drug effects
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Signal Transduction / physiology
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Transcription Factor AP-1 / biosynthesis*
Substances
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Glial Fibrillary Acidic Protein
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Proto-Oncogene Proteins c-fos
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Receptors, Purinergic P2
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Transcription Factor AP-1
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Adenosine Triphosphate
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Protein Kinase C