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Titolo:
Cardiomyopathy in mice with paternal uniparental disomy for chromosome 12
Autore:
Villar, AJ; Carlson, EJ; Gillespie, AM; Ursell, PC; Epstein, CJ;
Indirizzi:
Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94143 USA Univ Calif San Francisco San Francisco CA USA 94143 ancisco, CA 94143 USA Buck Ctr Res Aging, Novato, CA USA Buck Ctr Res Aging Novato CA USABuck Ctr Res Aging, Novato, CA USA Univ Calif San Francisco, Dept Pathol, San Francisco, CA 94143 USA Univ Calif San Francisco San Francisco CA USA 94143 ancisco, CA 94143 USA
Titolo Testata:
GENESIS
fascicolo: 4, volume: 30, anno: 2001,
pagine: 274 - 279
SICI:
1526-954X(200108)30:4<274:CIMWPU>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
SPONGY MYOCARDIUM; HUMAN-DISEASE; MOUSE; GENE; GTL2; EPICARDIUM; RECEPTOR; DEFECTS; ORIGIN;
Keywords:
genomic imprinting; chromosome 12; uniparental disomy; cardiomyopathy;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
31
Recensione:
Indirizzi per estratti:
Indirizzo: Villar, AJ Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94143 USA Univ Calif San Francisco San Francisco CA USA 94143 94143 USA
Citazione:
A.J. Villar et al., "Cardiomyopathy in mice with paternal uniparental disomy for chromosome 12", GENESIS, 30(4), 2001, pp. 274-279

Abstract

Mice inheriting both copies of MMU12 either maternally or paternally demonstrate imprinting effects. Whereas maternal uniparental disomy 12 (matUPD12) fetuses are growth retarded and die perinatally, paternal UPD12 (patUPD12) fetuses die during late gestation an exhibit placentomegaly and skeletal muscle maturation defects. To examine further the developmental consequences of UPD12, we intercrossed mouse stocks heterozygous; for Robertsonian translocation chromosomes (8.12) and (10.12). We report that at 13.5-14.5 dg patUPD12 hearts exhibit Increased ventricular diameter, thinner, less compact myocardium, and deep intertrabecular recesses when compared to controls. These data provide evidence for cardiac failure, a lethal condition and suggest a role for an imprinted gene(s) in normal heart development. (C) 2001 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/02/20 alle ore 15:10:14