Abstract
Specific mutations in the human gene encoding lamin A or in the lamin A-processing enzyme, Zmpste24, cause premature aging. New data on mice and humans suggest that these mutations affect adult stem cells by interfering with the Notch and Wnt signaling pathways.
Publication types
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Comment
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Research Support, Non-U.S. Gov't
MeSH terms
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Aging / metabolism*
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Animals
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Lamins / genetics
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Lamins / metabolism*
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Membrane Proteins / genetics
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Membrane Proteins / metabolism
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Metalloendopeptidases / genetics
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Metalloendopeptidases / metabolism
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Mice
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Progeria / metabolism*
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Receptors, Notch / metabolism
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Signal Transduction*
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Stem Cells / metabolism*
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Wnt Proteins / metabolism
Substances
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Lamins
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Membrane Proteins
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Receptors, Notch
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Wnt Proteins
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Metalloendopeptidases