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|Title:||Are transgenic mice the 'alkahest' to understanding myocardial hypertrophy and failure?||Authors:||Cook S.A.
|Keywords:||?-myosin heavy chain promoter
Extracellular signal-regulated kinase 1/2 cascade
Genetic background and strain effects
Glycogen synthase kinase 3
Protein kinase B/Akt
Ryanodine receptor 2
Signal strength matching
|Issue Date:||2009||Publisher:||ScienceDirect||Citation:||Cook S.A., Clerk A., Sugden P.H. (2009). Are transgenic mice the 'alkahest' to understanding myocardial hypertrophy and failure?. Journal of Molecular and Cellular Cardiology 46 (2) : 118-129. ScholarBank@NUS Repository. https://doi.org/10.1016/j.yjmcc.2008.11.005||Abstract:||Murine transgenesis using cardioselective promoters has become increasingly common in studies of cardiac hypertrophy and heart failure, with expression mediated by pronuclear microinjection being the commonest format. Without wishing to decry their usefulness, in our view, such studies are not necessarily as unambiguous as sometimes portrayed and clarity is not always their consequence. We describe broadly the types of approach undertaken in the heart and point out some of the drawbacks. We provide three arbitrarily-chosen examples where, in spite of a number of often-independent studies, no consensus has yet been achieved. These include glycogen synthase kinase 3, the extracellular signal-regulated kinase pathway and the ryanodine receptor 2. We believe that the transgenic approach should not be viewed in an empyreal light and, depending on the questions asked, we suggest that other experimental systems provide equal (or even more) valuable outcomes. � 2008 Elsevier Inc. All rights reserved.||Source Title:||Journal of Molecular and Cellular Cardiology||URI:||http://scholarbank.nus.edu.sg/handle/10635/149279||ISSN:||222828||DOI:||10.1016/j.yjmcc.2008.11.005|
|Appears in Collections:||Staff Publications|
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