Key result
Vangl2 mutation in Lp/Lp mice inhibits the polarization and migration of myocardializing cells into the outflow tract cushions by disrupting RhoA expression.
Vangl2 acts via the RhoA/ROCK1 signaling pathway to regulate polarized cell movements essential for proximal outflow tract development.
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Does not inform clinical management of outflow tract defects; leaves open Vangl2-RhoA signaling as a target for human validation.
Phillips et al. (2005) studied Double outlet right ventricle and aortic arch defects (Vangl2 mutation). Vangl2 mutation (Lp/Lp) vs. Wild-type fetuses was evaluated on Polarization and movement of myocardializing cells into the outflow tract cushions. Vangl2 mutation in Lp/Lp mice inhibits the polarization and migration of myocardializing cells into the outflow tract cushions by disrupting RhoA expression.
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