Literature DB >> 8621584

An alternative splicing product of the lamin A/C gene lacks exon 10.

B M Machiels1, A H Zorenc, J M Endert, H J Kuijpers, G J van Eys, F C Ramaekers, J L Broers.   

Abstract

Expression of the A-type lamins was studied in the lung adenocarcinoma cell line GLC-A1. A-type lamins, consisting of lamin A and C, are two products arising from the same gene by alternative splicing. Northern blotting showed in GLC-A1 a relatively low expression level of lamin C and an even lower expression level of lamin A as compared to other adenocarcinoma cell lines. Immunofluorescence studies revealed highly irregular nuclear inclusions of lamin A, suggesting protein or gene expression abnormalities. Reverse transcriptase-polymerase chain reaction-based cDNA analysis followed by sequencing indicated the presence of an as yet unidentified alternative splicing product of the lamin A/C gene. This product differs from lamin A by the absence of the 5' part of exon 10 (90 nucleotides). Therefore we propose to designate this product lamin Adelta10. Deletion of the 30 amino acids encoded by exon 10 was predicted to result in a shift in pI of the protein from 7.4 to approximately 8.6, which was confirmed by two-dimensional immunoblotting. mRNA analysis in a variety of cell lines, normal colon tissue as well as carcinomas demonstrated the presence of lamin Adelta 10 in all samples examined, suggesting its presence in a variety of cell types.

Entities:  

Mesh:

Substances:

Year:  1996        PMID: 8621584     DOI: 10.1074/jbc.271.16.9249

Source DB:  PubMed          Journal:  J Biol Chem        ISSN: 0021-9258            Impact factor:   5.157


  56 in total

1.  Expression of a mutant lamin A that causes Emery-Dreifuss muscular dystrophy inhibits in vitro differentiation of C2C12 myoblasts.

Authors:  Catherine Favreau; Dominique Higuet; Jean-Claude Courvalin; Brigitte Buendia
Journal:  Mol Cell Biol       Date:  2004-02       Impact factor: 4.272

Review 2.  Protein farnesylation and disease.

Authors:  Giuseppe Novelli; Maria Rosaria D'Apice
Journal:  J Inherit Metab Dis       Date:  2012-02-04       Impact factor: 4.982

Review 3.  Lamins at a glance.

Authors:  Chin Yee Ho; Jan Lammerding
Journal:  J Cell Sci       Date:  2012-05-01       Impact factor: 5.285

Review 4.  Skin Disease in Laminopathy-Associated Premature Aging.

Authors:  Tomás McKenna; Agustín Sola Carvajal; Maria Eriksson
Journal:  J Invest Dermatol       Date:  2015-07-29       Impact factor: 8.551

5.  Molecular diversity of rat brain proteins as revealed by proteomic analysis.

Authors:  Jae-Won Yang; Jean-François Juranville; Harald Höger; Michael Fountoulakis; Gert Lubec
Journal:  Mol Divers       Date:  2005       Impact factor: 2.943

Review 6.  Emery-Dreifuss muscular dystrophy.

Authors:  Antoine Muchir; Howard J Worman
Journal:  Curr Neurol Neurosci Rep       Date:  2007-01       Impact factor: 5.081

Review 7.  GFAP and its role in Alexander disease.

Authors:  Roy A Quinlan; Michael Brenner; James E Goldman; Albee Messing
Journal:  Exp Cell Res       Date:  2007-04-06       Impact factor: 3.905

Review 8.  Nuclear lamins: major factors in the structural organization and function of the nucleus and chromatin.

Authors:  Thomas Dechat; Katrin Pfleghaar; Kaushik Sengupta; Takeshi Shimi; Dale K Shumaker; Liliana Solimando; Robert D Goldman
Journal:  Genes Dev       Date:  2008-04-01       Impact factor: 11.361

9.  Increased expression of the Hutchinson-Gilford progeria syndrome truncated lamin A transcript during cell aging.

Authors:  Sofia Rodriguez; Fabio Coppedè; Hanna Sagelius; Maria Eriksson
Journal:  Eur J Hum Genet       Date:  2009-01-28       Impact factor: 4.246

10.  Increased noncanonical splicing of autoantigen transcripts provides the structural basis for expression of untolerized epitopes.

Authors:  Bernard Ng; Fan Yang; David P Huston; Yan Yan; Yu Yang; Zeyu Xiong; Leif E Peterson; Hong Wang; Xiao-Feng Yang
Journal:  J Allergy Clin Immunol       Date:  2004-12       Impact factor: 10.793

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.