Cardiac-specific deletion of Gata4 reveals its requirement for hypertrophy, compensation, and myocyte viability.

@article{Oka2006CardiacspecificDO,
  title={Cardiac-specific deletion of Gata4 reveals its requirement for hypertrophy, compensation, and myocyte viability.},
  author={Toru Oka and Marjorie Maillet and Alistair J. Watt and Robert J. Schwartz and Bruce J. Aronow and S A Duncan and Jeffery D Molkentin},
  journal={Circulation research},
  year={2006},
  volume={98 6},
  pages={837-45}
}
The transcription factor GATA4 is a critical regulator of cardiac gene expression where it controls embryonic development, cardiomyocyte differentiation, and stress responsiveness of the adult heart. Traditional deletion of Gata4 caused embryonic lethality associated with endoderm defects and cardiac malformations, precluding an analysis of the role of GATA4 in the adult myocardium. To address the function of GATA4 in the adult heart, Gata4-loxP-targeted mice (Gata4fl/fl) were crossed with mice… CONTINUE READING

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