Abstract
Activation of opioid receptors have been implicated in the modulation of cell proliferation and the E2F family of transcription factors may play a role in opioid inhibition of DNA synthesis. Gel shift assays and Western blotting of nuclear extracts from NG108-15 cells revealed increased E2F1 DNA binding activity and higher levels of E2F1 following activation of delta-opioid receptors. It is suggested that DADLE-induced regulation of E2F DNA binding activity involves ERKs.
MeSH terms
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Analgesics, Opioid / pharmacology*
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Animals
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Blotting, Western / methods
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Cell Cycle Proteins / metabolism*
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Cell Line, Tumor
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Cell Proliferation / drug effects
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DNA-Binding Proteins / metabolism*
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E2F Transcription Factors
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E2F1 Transcription Factor
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Electrophoretic Mobility Shift Assay / methods
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Enkephalin, Leucine-2-Alanine / pharmacology*
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Enzyme Inhibitors / pharmacology
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Flavonoids / pharmacology
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Flow Cytometry / methods
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Imidazoles / pharmacology
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Mice
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Neuroblastoma / pathology
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Protein Binding / drug effects
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Pyridines / pharmacology
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Receptors, Opioid, delta / drug effects*
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Thymidine / pharmacokinetics
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Transcription Factors / metabolism*
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Tritium / pharmacokinetics
Substances
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Analgesics, Opioid
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Cell Cycle Proteins
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DNA-Binding Proteins
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E2F Transcription Factors
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E2F1 Transcription Factor
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E2f1 protein, mouse
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Enzyme Inhibitors
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Flavonoids
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Imidazoles
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Pyridines
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Receptors, Opioid, delta
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Transcription Factors
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Tritium
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Enkephalin, Leucine-2-Alanine
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SB 203580
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2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one
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Thymidine