Key result
Myocardin optimally transactivates the human ACTG2 promoter by discriminating among juxtaposed CArG elements through a physical and functional partnership with the transcription factor NKX3.1.
Population
In vitro cell models (non-SMC cell type stably transfected with Myocd, human ACTG2 promoter constructs)
Comparison
Myocardin expression/transfection and mutation… vs Wild-type constructs, non-transfected cells…
Design
Preclinical
Authors
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Hypothesis-generating for smooth muscle differentiation mechanisms; leaves open relevance to human cardiovascular disease.
Myocardin optimally transactivates the human ACTG2 promoter through specific CArG elements and a novel partnership with NKX3.1, driving smooth muscle cell differentiation.
Sun et al. (2009) studied this question. Myocardin optimally transactivates the human ACTG2 promoter by discriminating among juxtaposed CArG elements through a physical and functional partnership with the transcription factor NKX3.1.
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