Myocardial deletion of Smad4 using a novel alpha skeletal muscle actin Cre recombinase transgenic mouse causes misalignment of the cardiac outflow tract

Azhar, M, Wang, PY, Frugier, T, Koishi, K, Deng, CX, Noakes, PG and McLennan, IS (2010) Myocardial deletion of Smad4 using a novel alpha skeletal muscle actin Cre recombinase transgenic mouse causes misalignment of the cardiac outflow tract. International Journal of Biological Sciences, 6 6: 546-555.

Attached Files (Some files may be inaccessible until you login with your UQ eSpace credentials)
Name Description MIMEType Size Downloads
UQ223504.pdf HERDC evidence - not publicly available application/pdf 1.00MB 5
UQ223504_OA.pdf Full text (open access) application/pdf 967.77KB 1
Author Azhar, M
Wang, PY
Frugier, T
Koishi, K
Deng, CX
Noakes, PG
McLennan, IS
Title Myocardial deletion of Smad4 using a novel alpha skeletal muscle actin Cre recombinase transgenic mouse causes misalignment of the cardiac outflow tract
Formatted title
Myocardial deletion of Smad4 using a novel alpha skeletal muscle actin Cre recombinase transgenic mouse causes misalignment of the cardiac outflow tract
Journal name International Journal of Biological Sciences   Check publisher's open access policy
ISSN 1449-2288
Publication date 2010-09-20
Sub-type Article (original research)
Open Access Status File (Publisher version)
Volume 6
Issue 6
Start page 546
End page 555
Total pages 10
Place of publication Lake Haven, NSW, Australia
Publisher Ivyspring International Publisher
Collection year 2011
Language eng
Formatted abstract
SMAD4 acts as the converging point for TGFβ and BMP signaling in heart development. Here, we investigated the role of SMAD4 in heart development using a novel α skeletal muscle actin Cre recombinase (MuCre) transgenic mouse strain. Lineage tracing using MuCre/ROSA26LacZ reporter mice indicated strong Cre-recombinase expression in developing and adult heart and skeletal muscles. In heart development, significant MuCre expression was noted at E11.5 in the atrial, ventricular, outflow tract and atrioventricular canal myocardium, but not in the endocardial cushions. MuCre-driven conditional deletion of Smad4 in mice caused double outlet right ventricle (DORV), ventricular septal defect (VSD), impaired trabeculation and thinning of ventricular myocardium, and mid-gestational embryonic lethality. In conclusion, MuCre mice effectively delete genes in both heart and skeletal muscles, thus enabling the discovery that myocardial Smad4 deletion causes misalignment of the outflow tract and DORV.
©Ivyspring International Publisher
Keyword Heart
Myogenesis
Transforming growth factor beta
SMAD
Marfan syndrome
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ
Additional Notes Published under Research Paper.

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2011 Collection
Queensland Brain Institute Publications
School of Biomedical Sciences Publications
 
Versions
Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 10 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 0 times in Scopus Article
Google Scholar Search Google Scholar
Created: Sun, 05 Dec 2010, 00:11:57 EST