Abstract
Microtubules are polymers of alpha/beta-tubulin participating in essential cell functions. A multistep process involving distinct molecular chaperones and cofactors produces new tubulin heterodimers competent to polymerise. In vitro cofactor A (TBCA) interacts with beta-tubulin in a quasi-native state behaving as a molecular chaperone. We have used siRNA to silence TBCA expression in HeLa and MCF-7 mammalian cell lines. TBCA is essential for cell viability and its knockdown produces a decrease in the amount of soluble tubulin, modifications in microtubules and G1 cell cycle arrest. In MCF-7 cells, cell death was preceded by a change in cell shape resembling differentiation.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Actin Cytoskeleton / metabolism
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Apoptosis* / drug effects
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Caspase 7
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Caspases / metabolism
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Cell Cycle* / drug effects
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G1 Phase / drug effects
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G1 Phase / genetics
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Gene Silencing
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HeLa Cells
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Humans
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Microtubule-Associated Proteins / genetics
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Microtubule-Associated Proteins / physiology*
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Microtubules / metabolism*
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Molecular Chaperones / genetics
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Molecular Chaperones / physiology*
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Phenotype
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RNA, Small Interfering / genetics
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RNA, Small Interfering / pharmacology
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Tubulin / metabolism
Substances
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Microtubule-Associated Proteins
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Molecular Chaperones
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RNA, Small Interfering
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TBCA protein, human
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Tubulin
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CASP7 protein, human
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Caspase 7
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Caspases