Journal article

A novel conditional mouse model for Nkx2-5 reveals transcriptional regulation of cardiac ion channels

Milena B Furtado, Julia C Wilmanns, Anjana Chandran, Mary Tonta, Christine Biben, Michael Eichenlaub, Harold A Coleman, Silke Berger, Romaric Bouveret, Reena Singh, Richard P Harvey, Mirana Ramialison, James T Pearson, Helena C Parkington, Nadia A Rosenthal, Mauro W Costa

DIFFERENTIATION | ELSEVIER SCI LTD | Published : 2016

Abstract

Nkx2-5 is one of the master regulators of cardiac development, homeostasis and disease. This transcription factor has been previously associated with a suite of cardiac congenital malformations and impairment of electrical activity. When disease causative mutations in transcription factors are considered, NKX2-5 gene dysfunction is the most common abnormality found in patients. Here we describe a novel mouse model and subsequent implications of Nkx2-5 loss for aspects of myocardial electrical activity. In this work we have engineered a new Nkx2-5 conditional knockout mouse in which flox sites flank the entire Nkx2-5 locus, and validated this line for the study of heart development, different..

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University of Melbourne Researchers

Grants

Awarded by NHMRC Project Grant


Awarded by NHMRC/NHF Career Development Fellowship


Awarded by ARC Discovery Project


Funding Acknowledgements

The Australian Regenerative Medicine Institute is supported by grants from the State Government of Victoria and the Australian Government. This work was also funded by NHMRC-Australia Fellowship to NAR and NHMRC Project Grant 1069710 to MWC and NAR, ARC Stem Cells Australia to NAR, NHMRC/NHF Career Development Fellowship 1049980 and ARC Discovery Project DP140101067 to MR, NHMRC Project Grant 1042478 to HP.