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Titolo:
Endothelium-specific replacement of the connexin43 coding region by a lacZreporter gene
Autore:
Theis, M; de Wit, C; Schlaeger, TM; Eckardt, D; Kruger, O; Doring, B; Risau, W; Deutsch, U; Pohl, U; Willecke, K;
Indirizzi:
Univ Bonn, Inst Genet, D-53117 Bonn, Germany Univ Bonn Bonn Germany D-53117 v Bonn, Inst Genet, D-53117 Bonn, Germany Univ Munich, Inst Physiol, D-8000 Munich, Germany Univ Munich Munich Germany D-8000 , Inst Physiol, D-8000 Munich, Germany Max Planck Inst Physiol & Clin Res, WG Kerckhoff Inst, Dept Mol Cell Biol,D-6350 Bad Nauheim, Germany Max Planck Inst Physiol & Clin Res Bad Nauheim Germany D-6350 m, Germany
Titolo Testata:
GENESIS
fascicolo: 1, volume: 29, anno: 2001,
pagine: 1 - 13
SICI:
1526-954X(200101)29:1<1:EROTCC>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
MICE LACKING CONNEXIN43; GAP-JUNCTIONS; TRANSGENIC MICE; EXPRESSION; CELLS; RECOMBINATION; CONDUCTION; COMMUNICATION; ARTERIOLES; DEFICIENT;
Keywords:
vascular endothelium; gap junctions; blood pressure; Cre/loxP system; cell autonomous expression;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Willecke, K Univ Bonn, Inst Genet, Romerstr 164, D-53117 Bonn, Germany Univ Bonn Romerstr 164 Bonn Germany D-53117 117 Bonn, Germany
Citazione:
M. Theis et al., "Endothelium-specific replacement of the connexin43 coding region by a lacZreporter gene", GENESIS, 29(1), 2001, pp. 1-13

Abstract

The murine gap junction protein connexin43 (Cx43) is expressed in blood vessels, with vastly different contribution by endothelial and smooth muscle cells. We have used the Cre recombinase under control of TIE2 transcriptional elements to inactivate a flexed Cx43 gene specifically in endothelial cells. Ore-mediated deletion led to replacement of the Cx43 coding region by a lacZ reporter gene. This allowed us to monitor the extent of deletion andto visualize the endothelial expression pattern of Cx43. We found widespread endothelial expression of the Cx43 gene during embryonic development, which became restricted largely to capillaries and small Vessels in all adultorgans examined. Mice lacking Cx43 in endothelium did not exhibit altered blood pressure, in contrast to mice deficient in Cx40. Our results show that lacZ activation after deletion of the target gene allows us to determine the extent of cell type-specific deletion after phenotypical investigation of the same animal. genesis 29:1-13, 2001. (C) 2001 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/01/21 alle ore 12:29:04