Abstract
The role of inhibition of prelamin A processing in the inhibition of DNA synthesis by lovastatin was examined by expressing prelamin A in F9 teratocarcinoma cells. These cells, normally lacking expression of the A/C lamins, were transfected with constructs expressing either prelamin A or mature lamin A and the effect of lovastatin on DNA biosynthesis was assessed. It was found that expression of prelamin A specifically conferred sensitivity to inhibition of DNA biosynthesis by lovastatin on F9 cells.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Cholesterol / biosynthesis
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Cricetinae
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DNA, Neoplasm / biosynthesis*
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Dexamethasone / pharmacology
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Dose-Response Relationship, Drug
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Gene Expression Regulation, Neoplastic / drug effects
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Humans
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Lamin Type A
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Lamins
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Lovastatin / pharmacology*
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Mevalonic Acid / metabolism
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Mice
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Nuclear Proteins / biosynthesis*
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Nuclear Proteins / genetics
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Protein Precursors / biosynthesis*
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Protein Precursors / genetics
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Protein Processing, Post-Translational
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Proto-Oncogene Proteins p21(ras) / isolation & purification
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Recombinant Proteins / biosynthesis
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Stem Cells
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Teratocarcinoma
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Transfection
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Tumor Cells, Cultured
Substances
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DNA, Neoplasm
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Lamin Type A
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Lamins
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Nuclear Proteins
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Protein Precursors
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Recombinant Proteins
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prelamin A
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Dexamethasone
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Cholesterol
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Lovastatin
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HRAS protein, human
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Proto-Oncogene Proteins p21(ras)
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Mevalonic Acid