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In this model, p53 expression level was increased and the phenotype was rescued following inhibition of p53.
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As predicted by the endo16 model, brn1/2/4 expression is confined perfectly to the midgut, coincident with the domain of endo16 expression.
In MPNST cells and in a genetically engineered mouse model, MEIS1 expression in developing nerve glial cells was necessary for MPNST growth.
These data show that in our cellular model PDE5 expression is responsive to insulin treatment.
In one model, Prkg1 expression was rescued only in smooth muscle (SM) cells of Prkg1 null mutants (Prkg1SMr mice) [21].
In an experimental breast cancer mouse model, VEGFR2 expression has been detected by Technetium-99m pertechnetate (Tc-99m) labeled VEGF [24].
Consistent with this model, Slit2 expression along with Shh in HEK293 effectively suppressed the chemoattractive activity of Shh towards mDN axons in explant cultures (Figure S1).
According to data reported by Menssen and colleagues [50] who demonstrated that MAD2 is transcriptionally regulated by Myc, in our model MAD2 expression levels increased when Myc was up-regulated, conversely a reduced expression of MAD2 was obtained in Myc cells.
In this model, CD74 expression was localized to podocytes [ 24].
By multivariate analysis (proportional hazards model), GAS6 expression was still an independent negative prognostic factor (P = 0.0028, likelihood ratio).
In this model, USF1 expression is higher in BALB than in B6 strain owing to a promoter polymorphism.
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