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Lamins as mediators of oxidative stress.

Abstract：

:The nuclear lamina defines both structural and functional properties of the eukaryotic cell nucleus. Mutations in the LMNA gene, encoding A-type lamins, lead to a broad spectrum of diseases termed laminopathies. While different hypotheses have been postulated to explain disease development, there is still no unified view on the mechanistic basis of laminopathies. Recent observations indicate that laminopathies are often accompanied by altered levels of reactive oxygen species and a higher susceptibility to oxidative stress at the cellular level. In this review, we highlight the role of reactive oxygen species for cell function and disease development in the context of laminopathies and present a framework of non-exclusive mechanisms to explain the reciprocal interactions between a dysfunctional lamina and altered redox homeostasis.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Sieprath T,Darwiche R,De Vos WH

doi

10.1016/j.bbrc.2012.04.058

subject

Has Abstract

pub_date

2012-05-18 00:00:00

pages

635-9

issue

4

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(12)00724-3

journal_volume

421

pub_type

杂志文章,评审

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