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Notably, studies in rat and mouse identified a number of stimuli or environmental conditions that alter expression of selected mRNAs in immature, or mature brain, in conjunction with often bidirectional changes in CpG methylation of the corresponding promoters [8], [9], [39], [40].

Prior characterization of the Hmx1 dm/dm mouse identified a microphthalmia phenotype in adults but did not quantify the reduction in eye size (Munroe et al., 2009).

Interestingly, a more recent study of an independently generated Agrp−/− mouse identified a modest late-onset lean phenotype with reduced body weight and adiposity after 6 months (27).

In light of these data, it was surprising that the first study of an Agrp−/− mouse identified a phenotype with normal locomotor activity, growth rates, body composition, food intake, and response to starvation (21).

Studies in the mouse identified a synthetic lethal interaction between mutant Kras and Cdk4, where Cdk4 ablation caused lung cells expressing mutant Kras to undergo senescence and prevented tumor growth [69].

No open reading frame (ORF) had been identified in this sequence yet, but the comparison of our dog sequence with the one from mouse identified a putative ORF on the basis that in the 385 bp-long region of similarity most of the differences occurred at the third position of base triplets in frame with a starting ATG codon.

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Utilizing DCs derived from complement receptor 3-deficient miCR3−/R3−/− mice) identified a requirement for CR3 in the internalization of both sham- and serum-coated particles.

A recent study in mice identified a disease-susceptibility polymorphism of the CTLA-4 gene affecting CTLA-4 splicing in exon 2.

Histological analysis of Rab18 −/− mice identified a delay in closure of the lens vesicle at E12.5 and abnormalities in denucleation of fibre cells in neonates (Fig. 2).

Lipidomic analyses of colonic tissue from eosinophil-deficient mice identified a deficiency in the docosahexaenoic acid-derived anti-inflammatory mediator 10, 17- dihydroxydocosahexaenoic acid (diHDoHE), namely protectin D1 (PD1).

A cDNA sequence comparison among susceptible and resistant strains of mice identified a single nucleotide substitution that causes a premature stop codon in the Oas1b transcripts of susceptible mice [ 12, 13].

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