Howard J. Worman, Jean-Claude Courvalin
J Clin Invest.
2004;
113(3):349–351
doi:10.1172/JCI20832
This article Copyright © 2004, The American Society for Clinical Investigation
Abstract
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utations in lamins A and C, nuclear intermediate-filament proteins in nearly all somatic cells, cause a variety of diseases that primarily affect striated muscle, adipocytes, or peripheral nerves or cause features of premature aging. Two new studies use lamin A/C–deficient mice, which develop striated muscle disease, as a model to investigate pathogenic mechanisms. These reports provide evidence for a stepwise process in which mechanically stressed cells first develop chromatin and nuclear envelope damage and then develop secondary alterations in the transcriptional activation of genes in adaptive and protective pathways.
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