Mutations in the gene that encodes nuclear lamins A and C cause a host of diseases, ranging from dilated cardiomyopathy to lipid disorders. The aging syndrome, Hutchinson-Gilford progeria, is now added to the list.
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References
Burke, B. & Stewart, C.L. Life at the edge: the nuclear envelope and human disease. Nat. Rev. Mol. Cell. Biol. 3, 575–585 (2002).
Worman, H.J. & Courvalin, J.C. The nuclear lamina and inherited disease. Trends Cell Biol. 12, 591–598 (2002).
Eriksson, M. et al. Recurrent de novo point mutations in lamin A cause Hutchinson-Gilford progeria syndrome. Nature 423, 293–298 (2003).
De Sandre-Giovannoli, A. et al. Lamin A truncation in Hutchinson-Gilford Progeria. Science, published online 17 April 2003 (doi:10.1126/science.1084125).
Cao, H. & Hegele, R.A. LMNA is mutated in Hutchinson-Gilford progeria (MIM 176670) but not in Wiedemann-Rautenstrauch progeroid syndrome (MIM 264090). J. Hum. Genet., published online 3 April 2003 (doi:10.1007/s10038-003-0025-3).
Mounkes, L.C. et al. A progeroid syndrome in mice is caused by defects in the A-type lamins. Nature 423, 298–301 (2003).
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Hegele, R. Lamin mutations come of age. Nat Med 9, 644–645 (2003). https://doi.org/10.1038/nm0603-644
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DOI: https://doi.org/10.1038/nm0603-644
