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Twist1-null mouse embryos exhibit failure of cephalic neural tube closure and abnormal head development and die at E11.0.
ICAT-deficient mouse embryos exhibit a smaller overall brain size and abnormal forebrain morphologies.
Cells derived from pp125FAK−/− mouse embryos exhibit reduced migration as a result of impaired adhesion turnover (Ilic et al, 1995, 1996).
Another potential difference between mouse models and human NTDs is that many gene-specific homozygous null mouse embryos exhibit phenotypes additional to NTDs, such as prenatally lethal heart defects.
Tex19.1 appears to play an important role in placenta function as Tex19.1 −/− mouse embryos exhibit intra-uterine growth retardation and have small placentas due to a reduction in the number of spongiotrophoblast, glycogen trophoblast and sinusoidal trophoblast giant cells.
The importance of FAK in epithelial cell biology is underlined by the findings that epithelial cells lines expressing constitutively active FAK survive in suspension and that cells derived from FAK-/ mouse embryos exhibit reduced migration [ 8, 9].
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Moreover, E11.5 palladin KO mouse embryos exhibited markedly impaired differentiation of vascular SMC.
While Pofut1-deficient mouse embryos exhibited similar phenotype as Rbpj-deficient embryos [12], [33], postnatal phenotypes between Pofut1 and Rbpj mutant mice have varied depending on the experimental context.
Notch1 null mouse embryos exhibits significantly delayed and disorganized somitogenesis.
At 12.5 dpc, mouse embryos exhibited intense 5-hmC staining in a range of embryonic tissues.
We confirm here that compared to wildtype mice (Fig. 1a) heart looping in the Talpid3 − / − mouse at E9.5 stage is randomized (Fig. 1b ..08% of Talpid3 − / − mouse embryos exhibited normal dextral looping (n = 19), 19.23% exhibited reversed, leftwards looping (n = 5) and 7.69% failed to undergo looping (n = 2).
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