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Selected Publication:

Type of publication: Journal Article
Type of document: Full Paper

Year: 2010

Authors: Wakula, P; Bisping, E; Kockskämper, J; Post, H; Brauer, S; Deuter, M; Oehlmann, R; Besenfelder, U; Lai, FA; Brem, G; Pieske, B

Title: CMV promoter is inadequate for expression of mutant human RyR2 in transgenic rabbits.

Source: J Pharmacol Toxicol Methods. 2010; 63(2):180-185

Authors Vetmeduni Vienna:

Besenfelder Urban
Brem Gottfried

Fundamental differences in Ca²+ homeostasis between mice and larger mammals require the validation of the mechanisms of arrhythmogenesis before translation into human pathophysiology. The purpose of this study was to create transgenic rabbits that express defective human cardiac ryanodine receptor (hRyR2) with a mutation (R4497C) causing a clinically relevant arrhythmogenic syndrome.

Keywords Pubmed: Animals
Animals, Genetically Modified/genetics*
Gene Expression
Green Fluorescent Proteins/biosynthesis
Green Fluorescent Proteins/chemistry
Green Fluorescent Proteins/genetics
Promoter Regions, Genetic*
RNA, Messenger/biosynthesis
RNA, Messenger/genetics
Recombinant Fusion Proteins/biosynthesis
Recombinant Fusion Proteins/chemistry
Recombinant Fusion Proteins/genetics
Reverse Transcriptase Polymerase Chain Reaction/methods
Ryanodine Receptor Calcium Release Channel/biosynthesis*
Ryanodine Receptor Calcium Release Channel/genetics*
Tachycardia, Ventricular/genetics
Tachycardia, Ventricular/metabolism

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