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Titolo:
The A-type lamins - Nuclear structural proteins as a focus for muscular dystrophy and cardiovascular diseases
Autore:
Mounkes, LC; Burke, B; Stewart, CL;
Indirizzi:
NCI, Lab Canc & Dev Biol, FCRDC, Frederick, MD 21702 USA NCI Frederick MDUSA 21702 anc & Dev Biol, FCRDC, Frederick, MD 21702 USA Univ Calgary, Dept Cell Biol & Anat, Calgary, AB, Canada Univ Calgary Calgary AB Canada ept Cell Biol & Anat, Calgary, AB, Canada
Titolo Testata:
TRENDS IN CARDIOVASCULAR MEDICINE
fascicolo: 7, volume: 11, anno: 2001,
pagine: 280 - 285
SICI:
1050-1738(200110)11:7<280:TAL-NS>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
FAMILIAL PARTIAL LIPODYSTROPHY; CAUSE AUTOSOMAL-DOMINANT; DILATED CARDIOMYOPATHY; A/C GENE; MISSENSE MUTATIONS; CONDUCTION-SYSTEM; DUNNIGAN VARIETY; C2 DOMAIN; EXPRESSION; MEMBRANE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Stewart, CL NCI, Lab Canc & Dev Biol, FCRDC, POB B, Frederick, MD 21702 USA NCI POB B Frederick MD USA 21702 OB B, Frederick, MD 21702 USA
Citazione:
L.C. Mounkes et al., "The A-type lamins - Nuclear structural proteins as a focus for muscular dystrophy and cardiovascular diseases", TREND CARD, 11(7), 2001, pp. 280-285

Abstract

Mutations in the lamin A (LMNA) gene are associated with the tissue-specific diseases Emery-Dreifuss muscular dystrophy (EDMD), limb girdle muscular dystrophy (LGMD-1B), dilated cardiomyopathy with conduction system disease (DCM-CD), and Dunnigan's familial partial lipodystrophy (FPLD). Lamins A and C, the products of the LMNA gene, are nuclear intermediate filament proteins and are the major structural components of the lamina network that underlies and supports the nuclear envelope. Nuclear fragility and mislocalization of the nuclear envelope protein emerin are two defects induced by a lack of the A-type lamins. These observations reveal that organization and structural integrity of the nucleus are critical factors in the origins of certain dystrophic and cardiovascular diseases. (Trends Cardiovasc Med 2001; 11:280-285). (C) 2001, Elsevier Science Inc.

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Documento generato il 06/07/20 alle ore 07:19:35