Heterozygous LmnadelK32 mice develop dilated cardiomyopathy through a combined pathomechanism of haploinsufficiency and peptide toxicity-Reference-Cited by-同舟云学术

Heterozygous LmnadelK32 mice develop dilated cardiomyopathy through a combined pathomechanism of haploinsufficiency and peptide toxicity

Published:2013-04-10 Issue:15 Volume:22 Page:3152-3164
ISSN:1460-2083
Container-title:Human Molecular Genetics
language:en
Short-container-title:

Author:

Cattin Marie-Elodie,Bertrand Anne T.,Schlossarek Saskia,Le Bihan Marie-Catherine,Skov Jensen Søren,Neuber Christiane,Crocini Claudia,Maron Sophia,Lainé Jeanne,Mougenot Nathalie,Varnous Shaïda,Fromes Yves,Hansen Arne,Eschenhagen Thomas,Decostre Valérie,Carrier Lucie,Bonne Gisèle

Publisher

Oxford University Press (OUP)

Subject

Genetics(clinical),Genetics,Molecular Biology,General Medicine

Link

http://academic.oup.com/hmg/article-pdf/22/15/3152/17260382/ddt172.pdf

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3. Missense mutations in the rod domain of the lamin A/C gene as causes of dilated cardiomyopathy and conduction-system disease;Fatkin;N. Engl. J. Med.,1999

4. ‘Laminopathies’: a wide spectrum of human diseases;Worman;Exp. Cell. Res.,2007

5. De novo LMNA mutations cause a new form of congenital muscular dystrophy;Quijano-Roy;Ann. Neurol.,2008

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