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Do Lamin A and Lamin C Have Unique Roles?

Overview
Journal Chromosoma
Specialty Molecular Biology
Date 2014 Oct 7
PMID 25283634
Citations 13
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Abstract

The A-type lamins, lamin A and lamin C, generated from a single gene, LMNA, are major structural components of the nuclear lamina. The two alternative splice products have mostly been studied together because they have been considered to be interchangeable. However, several lines of evidence indicate that in spite of being generated from the same gene and having high similarities in their primary sequences, the two isoforms are not equivalent in different biological aspects in both health and disease. The key question is whether they have both overlapping and unique functions and whether they are distinctly regulated. Based on the so far available experimental evidence, lamin A appears to be the most regulated A-type isoform during development, aging, and disease which indicates that lamin A is implicated in many different biological aspects and may have a greater repertoire of specialized functions than lamin C. The aim of this review is to point out differences between the two major LMNA splice variants and the consequences of these differences on their functions. This may guide further research and be of prime importance for the understanding of the pathogenesis of LMNA mutations.

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References
1.
Lopez-Mejia I, de Toledo M, Chavey C, Lapasset L, Cavelier P, Lopez-Herrera C . Antagonistic functions of LMNA isoforms in energy expenditure and lifespan. EMBO Rep. 2014; 15(5):529-39. PMC: 4210101. DOI: 10.1002/embr.201338126. View

2.
Mory P, Crispim F, Freire M, Salles J, Valerio C, Godoy-Matos A . Phenotypic diversity in patients with lipodystrophy associated with LMNA mutations. Eur J Endocrinol. 2012; 167(3):423-31. DOI: 10.1530/EJE-12-0268. View

3.
Sylvius N, Hathaway A, Boudreau E, Gupta P, Labib S, Bolongo P . Specific contribution of lamin A and lamin C in the development of laminopathies. Exp Cell Res. 2008; 314(13):2362-75. PMC: 3934841. DOI: 10.1016/j.yexcr.2008.04.017. View

4.
Broers J, Kuijpers H, Ostlund C, Worman H, Endert J, Ramaekers F . Both lamin A and lamin C mutations cause lamina instability as well as loss of internal nuclear lamin organization. Exp Cell Res. 2005; 304(2):582-92. DOI: 10.1016/j.yexcr.2004.11.020. View

5.
Melcer S, Gruenbaum Y, Krohne G . Invertebrate lamins. Exp Cell Res. 2007; 313(10):2157-66. DOI: 10.1016/j.yexcr.2007.03.004. View