Abstract
In this issue of Molecular Cell, Kim et al. (2009) describe the steps involved in the direct activation of the proapoptotic proteins BAX and BAK by their BH3-only partners, resolving the controversy regarding direct versus indirect activation of these proteins.
MeSH terms
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Animals
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Apoptosis Regulatory Proteins / metabolism
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Apoptosis*
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BH3 Interacting Domain Death Agonist Protein / metabolism
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Bcl-2-Like Protein 11
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Cells, Cultured
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Fibroblasts / cytology
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Fibroblasts / metabolism
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Membrane Proteins / metabolism
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Mice
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Mice, Knockout
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Mitochondria / metabolism*
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Models, Biological
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Protein Binding
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Protein Multimerization
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Proto-Oncogene Proteins / metabolism
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Tumor Suppressor Proteins / metabolism
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bcl-2 Homologous Antagonist-Killer Protein / chemistry
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bcl-2 Homologous Antagonist-Killer Protein / genetics
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bcl-2 Homologous Antagonist-Killer Protein / metabolism*
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bcl-2-Associated X Protein / chemistry
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bcl-2-Associated X Protein / genetics
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bcl-2-Associated X Protein / metabolism*
Substances
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Apoptosis Regulatory Proteins
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BH3 Interacting Domain Death Agonist Protein
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Bak1 protein, mouse
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Bax protein, mouse
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Bcl-2-Like Protein 11
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Bcl2l11 protein, mouse
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Membrane Proteins
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PUMA protein, mouse
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Proto-Oncogene Proteins
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Tumor Suppressor Proteins
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bcl-2 Homologous Antagonist-Killer Protein
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bcl-2-Associated X Protein