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Mice expressing a truncated ameloblastin (lacking exons 5 and 6), share similar histopathological features to the Y64H amelogenin mutant mice reported here (8, 31).
All class II/III PI3K mutant mice reported to date were created by gene targeting approaches that remove the protein of interest but do not allow the discrimination between scaffold- and kinase-dependent functions of these enzymes (Vanhaesebroeck et al., 2005).
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Third, studies on telomerase-deficient mutant mice report that after the fourth generation these mice have shorter telomeres and a number of impairments, including reduced viability, decreased proliferative capacity of B and T lymphocytes and various diseases [20].
However, analysis of a Nrarp null mutant mouse reported vascular patterning defects in the retina (Phng et al., 2009) and normal progression of the segmentation clock (Wright et al., 2009).
The first double-mutant mice reported, Fanca −/− Fancc −/−, show no evidence of an additive phenotype, suggesting an epistatic relationship between the two genes (Noll et al., 2002).
A previous study using mutant Seipin transgenic mice reported that the development of progressive motor deficits was associated with ER stress.
The "early-bird" phenotype in the mutant mice originally reported in this paper supposed that PACAP also has a critical role in daily behavioral patterns, especially during the light-to-dark transition period.
Furthermore, the incidence of pituitary tumors in the compound mutant mice was reported to be approximately 30% lower than that in the Rb1 +/− mice 10 and this reduced incidence was recapitulated in the Rb1 D326V/+ mutant mice (Fig. 8c, e).
The two top-ranked genes for gonadal dysgenesis, ZFX and ZFY, are known to function in sex differentiation and Zfx mutant mice are reported to have fewer germ cells than wild-type mice [ 45].
Previous studies using PS1 mutant-transgenic mice report that the magnitude of the increase in the relative Aβ42 level in cultured cells reflect the magnitude of increase in the brain (Borchelt et al, 1996; Citron et al, 1997).
Recently, a catalytically inactive IRAK1 D359A mutant mouse was reported (Pauls et al, 2013).
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