(Q50775986)

19 March 2018

title

Both lamin A and lamin C mutations cause lamina instability as well as loss of internal nuclear lamin organization (English)

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19 March 2018

author name string

Jos L V Broers

1

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19 March 2018

H J H Kuijpers

2

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19 March 2018

C Ostlund

3

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19 March 2018

H J Worman

4

1 reference

19 March 2018

J Endert

5

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19 March 2018

F C S Ramaekers

6

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19 March 2018

language of work or name

English

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publication date

20 December 2004

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19 March 2018

Experimental Cell Research

published in

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19 March 2018

volume

304

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19 March 2018

issue

2

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19 March 2018

page(s)

582-592

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19 March 2018

Dynamics and mobility of nuclear envelope proteins in interphase and mitotic cells revealed by green fluorescent protein chimeras

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The gene for a novel human lamin maps at a highly transcribed locus of chromosome 19 which replicates at the onset of S-phase.

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

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How do mutations in lamins A and C cause disease?

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Lamin A and ZMPSTE24 (FACE-1) defects cause nuclear disorganization and identify restrictive dermopathy as a lethal neonatal laminopathy

7 January 2021

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Nuclear envelope alterations in fibroblasts from LGMD1B patients carrying nonsense Y259X heterozygous or homozygous mutation in lamin A/C gene

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Loss of A-type lamin expression compromises nuclear envelope integrity leading to muscular dystrophy

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Effect of pathogenic mis-sense mutations in lamin A on its interaction with emerin in vivo

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Mutations in the gene encoding lamin A/C cause autosomal dominant Emery-Dreifuss muscular dystrophy

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Clinical and molecular genetic spectrum of autosomal dominant Emery-Dreifuss muscular dystrophy due to mutations of the lamin A/C gene

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Nuclear lamin A/C R482Q mutation in canadian kindreds with Dunnigan-type familial partial lipodystrophy

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LMNA, encoding lamin A/C, is mutated in partial lipodystrophy.

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The Ig-like structure of the C-terminal domain of lamin A/C, mutated in muscular dystrophies, cardiomyopathy, and partial lipodystrophy

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Expression of lamin A mutated in the carboxyl-terminal tail generates an aberrant nuclear phenotype similar to that observed in cells from patients with Dunnigan-type partial lipodystrophy and Emery-Dreifuss muscular dystrophy

7 January 2021

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Partial cleavage of A-type lamins concurs with their total disintegration from the nuclear lamina during apoptosis

7 January 2021

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cDNA sequencing of nuclear lamins A and C reveals primary and secondary structural homology to intermediate filament proteins

7 January 2021

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Cell cycle changes in A-type lamin associations detected in human dermal fibroblasts using monoclonal antibodies

7 January 2021

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The nuclear lamina is a meshwork of intermediate-type filaments

7 January 2021

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In vitro assembly properties of mutant and chimeric intermediate filament proteins: insight into the function of sequences in the rod and end domains of IF

7 January 2021

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Review: lamina-associated polypeptide 2 isoforms and related proteins in cell cycle-dependent nuclear structure dynamics

7 January 2021

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Nesprin-1alpha self-associates and binds directly to emerin and lamin A in vitro

7 January 2021

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The laminopathies: nuclear structure meets disease

7 January 2021

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Interphase nuclei of many mammalian cell types contain deep, dynamic, tubular membrane-bound invaginations of the nuclear envelope

7 January 2021

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7 January 2021

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Defects in nuclear structure and function promote dilated cardiomyopathy in lamin A/C-deficient mice

7 January 2021

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7 January 2021

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7 January 2021

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7 January 2021

based on heuristic

Effects of expressing lamin A mutant protein causing Emery-Dreifuss muscular dystrophy and familial partial lipodystrophy in HeLa cells

1 reference

https://api.crossref.org/works/10.1016%2FJ.YEXCR.2004.11.020

Failure of lamin A/C to functionally assemble in R482L mutated familial partial lipodystrophy fibroblasts: altered intermolecular interaction with emerin and implications for gene transcription

7 January 2021

1 reference

https://api.crossref.org/works/10.1016%2FJ.YEXCR.2004.11.020

Nuclear pore complexes form immobile networks and have a very low turnover in live mammalian cells

7 January 2021

1 reference

https://api.crossref.org/works/10.1016%2FJ.YEXCR.2004.11.020

A- and B-type lamins are differentially expressed in normal human tissues

7 January 2021

1 reference

https://api.crossref.org/works/10.1016%2FJ.YEXCR.2004.11.020

Crystal structure of the human lamin A coil 2B dimer: implications for the head-to-tail association of nuclear lamins

7 January 2021

1 reference

https://api.crossref.org/works/10.1016%2FJ.YEXCR.2004.11.020

The carboxyl-terminal region common to lamins A and C contains a DNA binding domain.

7 January 2021

1 reference

https://api.crossref.org/works/10.1016%2FJ.YEXCR.2004.11.020

Lamin A/C deficiency causes defective nuclear mechanics and mechanotransduction.

7 January 2021

1 reference

https://api.crossref.org/works/10.1016%2FJ.YEXCR.2004.11.020

Decreased mechanical stiffness in LMNA-/- cells is caused by defective nucleo-cytoskeletal integrity: implications for the development of laminopathies.

7 January 2021

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Spatial relationships in early signaling events of flow-mediated endothelial mechanotransduction

7 January 2021

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A-type lamins regulate retinoblastoma protein function by promoting subnuclear localization and preventing proteasomal degradation

7 January 2021

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https://api.crossref.org/works/10.1016%2FJ.YEXCR.2004.11.020

The retinoblastoma gene product is a cell cycle-dependent, nuclear matrix-associated protein

7 January 2021

1 reference

https://api.crossref.org/works/10.1016%2FJ.YEXCR.2004.11.020

A novel interaction between lamin A and SREBP1: implications for partial lipodystrophy and other laminopathies

7 January 2021

1 reference

https://api.crossref.org/works/10.1016%2FJ.YEXCR.2004.11.020

Transcriptional repressor germ cell-less (GCL) and barrier to autointegration factor (BAF) compete for binding to emerin in vitro

7 January 2021

1 reference

https://api.crossref.org/works/10.1016%2FJ.YEXCR.2004.11.020

In vivo and in vitro interaction between human transcription factor MOK2 and nuclear lamin A/C.

7 January 2021

1 reference

https://api.crossref.org/works/10.1016%2FJ.YEXCR.2004.11.020

10.1016/J.YEXCR.2004.11.020

7 January 2021

Identifiers

DOI

1 reference

19 March 2018

1 reference

19 March 2018