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Scientific article
Open access
English

Remodeling of gap junctions in mouse hearts hypertrophied by forced retinoic acid signaling

Published inJournal of Molecular and Cellular Cardiology, vol. 34, no. 10, p. 1411-1423
Publication date2002
Abstract

Beta-MHC-hRARalpha transgenic mice express a constitutively active (truncated) form of the human retinoic acid receptor which triggers development of dilated cardiomyopathy. In those hearts, we studied expression of gap junction proteins in relation to electrical impulse propagation.

Keywords
  • Actins/metabolism
  • Animals
  • Biomarkers/analysis
  • Blotting, Western
  • Body Weight
  • Cadherins/metabolism
  • Cardiomegaly/pathology
  • Connexin 43/metabolism
  • Cytoskeletal Proteins/metabolism
  • Down-Regulation
  • Electric Stimulation
  • Electrocardiography
  • Gap Junctions/metabolism
  • Mice
  • Mice, Transgenic
  • Myocardium/pathology
  • Organ Size
  • Receptors, Retinoic Acid/genetics/metabolism
  • Signal Transduction
  • Trans-Activators/metabolism
  • Tretinoin/metabolism
  • beta Catenin
Citation (ISO format)
VAN VEEN, Toon A B et al. Remodeling of gap junctions in mouse hearts hypertrophied by forced retinoic acid signaling. In: Journal of Molecular and Cellular Cardiology, 2002, vol. 34, n° 10, p. 1411–1423. doi: 10.1006/jmcc.2002.2102
Main files (1)
Article (Published version)
accessLevelPublic
Identifiers
ISSN of the journal0022-2828
92views
310downloads

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