Sentence examples for mice shared a from inspiring English sources

Abate-Shen showed that prostate tumors from low-testosterone mutant mice shared a similar gene expression profile to androgen-independent prostate tumors [ 50].

Comparisons of the knockout mouse liver tumor expression profiles with those induced by ciprofibrate or diethylnitrosamine showed that these mice shared a number of deregulated (up- or down-regulated) genes with ciprofibrate-induced liver tumors.

With prolonged NPC1-YFP induction, the majority of macrophages in the livers of R; N; Npc1 −/− mice shared a resting state morphology equivalent to macrophages found in wild-type mice.

The phenotypes of the Hi- and Lo-MYC mice share a number of similarities with the human disease.

Taken together, these suggest that humans and mice share a single locus encompassing one gene that may control corpus callosum development.

Earlier analyses of genomes showed that humans and mice share a similar repertoire of nGPCRs and encode about 367 and 392 nGPCRs, respectively, belonging to rhodopsin (class A), secretin receptor (class B), GABA receptor (class C), and Frizzled receptor (class F) classes [19], [22], [23].

After 21 d, mice were divided into balanced groups with mice sharing a divider cage placed in the same experimental group.

Interestingly, FGF21-Tg mice share a number of phenotypes with these long-lived mice including small size, enhanced insulin sensitivity and a blunted GH/IGF-1 signaling axis.

A/J and C57BL/6 J (B6) mice share a mutation in Cdh23 (ahl allele) and are characterized by age-related hearing loss.

Further proof that the myopathies described in ostes and Tg Pkd1l2) homozygous mice share a common pathogenic mechanism could be obtained from making double heterozygotes.

Mice overexpressing a truncated mutant of p53 (p53+/m, C-terminal part) or ΔNp63α were shown to exhibit a premature ageing of skin and shortened life span suggesting that these mice share a common molecular mechanism underlying these phenotypes [ 29, 30].