Key result
Expression of motor-impaired NMII-B in mice causes embryonic lethality at day 14.5 due to cardiac failure, cleft palate, ectopia cordis, and omphalocele via a dominant-negative effect.
A point mutation causing motor-impaired NMII-B results in a dominant-negative gain-of-function that disrupts normal ventral body wall closure and cardiac outflow tract development in mice.
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NMII-B ablation yields cardiac defects in mice; leaves open its role in human congenital heart disease.
Ma et al. (2014) studied Heart development and body wall closure defects. Expression of motor-deficient NMII-B (point mutant knock-in) vs. NMII-B null and hypomorphic mice was evaluated on Cardiac failure, midline fusion defects, and outflow tract myocardialization. Expression of motor-impaired NMII-B in mice causes embryonic lethality at day 14.5 due to cardiac failure, cleft palate, ectopia cordis, and omphalocele via a dominant-negative effect.
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