Abstract
Interference with the alternative splicing of apoptotic factors offers an innovative and specific mechanism to target malignant cells. In this issue of Chemistry & Biology, Zhou et al. report on the regulation of the alternative splicing of Bcl-x pre-mRNA in response to emetine, a potent protein synthesis inhibitor, as well as define a major player in the signaling mechanism.
MeSH terms
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Alternative Splicing / drug effects*
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Apoptosis / drug effects
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Cell Line, Tumor
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Emetine / pharmacology*
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Enzyme Inhibitors / pharmacology
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Gene Expression Regulation, Neoplastic / drug effects
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Humans
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Models, Biological
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Neoplasms / genetics
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Neoplasms / metabolism
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Neoplasms / pathology
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Protein Phosphatase 1 / antagonists & inhibitors
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Protein Phosphatase 1 / metabolism
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Signal Transduction / drug effects
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bcl-X Protein / genetics*
Substances
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Enzyme Inhibitors
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bcl-X Protein
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Protein Phosphatase 1
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Emetine