Literature DB >> 12661041

Nuclear envelope proteins and neuromuscular diseases.

Cecilia Ostlund1, Howard J Worman.   

Abstract

Several neuromuscular diseases are caused by mutations in emerin and A-type lamins, proteins of the nuclear envelope. Emery-Dreifuss muscular dystrophy is caused by mutations in emerin (X-linked) or A-type lamins (autosomal dominant). Mutations in A-type lamins also cause limb-girdle muscular dystrophy type 1B, dilated cardiomyopathy with conduction defect, and Charcot-Marie-Tooth disorder type 2B1. They also cause partial lipodystrophy syndromes. The functions of emerin and A-type lamins and the mechanisms of how mutations in these proteins cause tissue-specific diseases are not well understood. The mutated proteins may cause structural damage to cells but may also affect processes such as gene regulation. This review gives an overview of this topic and describes recent advances in identification of disease-causing mutations, studies of cells and tissues from subjects with these diseases, and animal and cell culture models.

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Year:  2003        PMID: 12661041     DOI: 10.1002/mus.10302

Source DB:  PubMed          Journal:  Muscle Nerve        ISSN: 0148-639X            Impact factor:   3.217


  21 in total

1.  An emerin "proteome": purification of distinct emerin-containing complexes from HeLa cells suggests molecular basis for diverse roles including gene regulation, mRNA splicing, signaling, mechanosensing, and nuclear architecture.

Authors:  James M Holaska; Katherine L Wilson
Journal:  Biochemistry       Date:  2007-07-10       Impact factor: 3.162

Review 2.  The muscular dystrophies: from genes to therapies.

Authors:  Richard M Lovering; Neil C Porter; Robert J Bloch
Journal:  Phys Ther       Date:  2005-12

3.  Skeletal myopathy in a family with lamin A/C cardiac disease.

Authors:  Subha Ghosh; Rahul Renapurkar; Subha V Raman
Journal:  Cardiovasc Diagn Ther       Date:  2016-10

4.  LMNA gene single nucleotide polymorphisms in dilated cardiomyopathy of Han children.

Authors:  Li-Jian Xie; Ting-Ting Xiao; Min Huang; Jie Shen
Journal:  Int J Clin Exp Med       Date:  2015-07-15

5.  The nuclear pore complex protein Tpr is a common autoantigen in sera that demonstrate nuclear envelope staining by indirect immunofluorescence.

Authors:  Y Ou; P Enarson; J B Rattner; S G Barr; M J Fritzler
Journal:  Clin Exp Immunol       Date:  2004-05       Impact factor: 4.330

6.  Lamin B1 mediates cell-autonomous neuropathology in a leukodystrophy mouse model.

Authors:  Mary Y Heng; Shu-Ting Lin; Laure Verret; Yong Huang; Sherry Kamiya; Quasar S Padiath; Ying Tong; Jorge J Palop; Eric J Huang; Louis J Ptáček; Ying-Hui Fu
Journal:  J Clin Invest       Date:  2013-05-15       Impact factor: 14.808

7.  TorsinA in the nuclear envelope.

Authors:  Teresa V Naismith; John E Heuser; Xandra O Breakefield; Phyllis I Hanson
Journal:  Proc Natl Acad Sci U S A       Date:  2004-05-10       Impact factor: 11.205

Review 8.  Autoantigens of the nuclear pore complex.

Authors:  P Enarson; J B Rattner; Y Ou; K Miyachi; T Horigome; M J Fritzler
Journal:  J Mol Med (Berl)       Date:  2004-06-03       Impact factor: 4.599

9.  Lamin B1 is required for mouse development and nuclear integrity.

Authors:  Laurent Vergnes; Miklós Péterfy; Martin O Bergo; Stephen G Young; Karen Reue
Journal:  Proc Natl Acad Sci U S A       Date:  2004-07-01       Impact factor: 11.205

10.  Reduced expression of lamin A/C correlates with poor histological differentiation and prognosis in primary gastric carcinoma.

Authors:  Zhengrong Wu; Lirong Wu; Desheng Weng; Dazhi Xu; Jian Geng; Fei Zhao
Journal:  J Exp Clin Cancer Res       Date:  2009-01-15
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