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• W2156812533 abstract "During recent years a number of severe clinical syndromes, collectively termed laminopathies, turned out to be caused by various, distinct mutations in the human LMNA gene. Arising from this, remarkable progress has been made to unravel the molecular pathophysiology underlying these disorders. A great benefit in this context was the generation of an A-type lamin deficient mouse line (Lmna−/−) by Sullivan and others,Citation1 which has become one of the most frequently used models in the field and provided profound insights to many different aspects of A-type lamin function. Here, we report the unexpected finding that these mice express a truncated Lmna gene product on both transcriptional and protein level. Combining different approaches including mass spectrometry, we precisely define this product as a C-terminally truncated lamin A mutant that lacks domains important for protein interactions and post-translational processing. Based on our findings we discuss implications for the interpretation of previous studies using Lmna−/− mice and the concept of human laminopathies." @default.
• W2156812533 created "2016-06-24" @default.
• W2156812533 creator A5003968059 @default.
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• W2156812533 date "2012-09-01" @default.
• W2156812533 modified "2023-10-16" @default.
• W2156812533 title "A truncated lamin A in the Lmna^−/−mouse line" @default.
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