LMNA mutations in cardiac transplant recipients. (Q54693639)

2 June 2018

title

LMNA mutations in cardiac transplant recipients. (English)

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2 June 2018

7

Axel Haverich

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2 June 2018

Klaus Pethig

1

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2 June 2018

Janine Genschel

2

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Tina Peters

3

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2 June 2018

Mathias Wilhelmi

4

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Peer Flemming

5

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Herbert Lochs

6

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Hartmut H-J Schmidt

8

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2 June 2018

language of work or name

English

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publication date

10 November 2004

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2 June 2018

published in

Cardiology

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2 June 2018

volume

103

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2 June 2018

page(s)

57-62

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2 June 2018

issue

2

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Report of the 1995 World Health Organization/International Society and Federation of Cardiology Task Force on the Definition and Classification of cardiomyopathies.

cites work

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Desmin mutation responsible for idiopathic dilated cardiomyopathy

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A R644C mutation within lamin A extends the mutations causing dilated cardiomyopathy.

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

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Mandibuloacral dysplasia is caused by a mutation in LMNA-encoding lamin A/C

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Lamin a truncation in Hutchinson-Gilford progeria.

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Recurrent de novo point mutations in lamin A cause Hutchinson–Gilford progeria syndrome

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Familial dilated cardiomyopathy and isolated left ventricular noncompaction associated with lamin A/C gene mutations.

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Disruption of nuclear lamin organization alters the distribution of replication factors and inhibits DNA synthesis

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A structural scaffolding of intermediate filaments in health and disease

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Implications of intermediate filament protein phosphorylation

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Loss of lamin A/C expression revealed by immuno-electron microscopy in dilated cardiomyopathy with atrioventricular block caused by LMNA gene defects.

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Functional consequences of an LMNA mutation associated with a new cardiac and non-cardiac phenotype

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Identifiers

DOI

10.1159/000082048

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2 June 2018

PubMed ID

15539782

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2 June 2018