Sentence examples for mouse models reviewed from inspiring English sources

Recently, it was reported that the NF-κB pathway is important for B-CLL in transgenic mouse models (reviewed in [9]), and that TCL1A activates NF-κB through an AKT-independent route [10].

Recently implicated directly in cancer initiation and/or progression using mouse models (reviewed in [39]), microRNAs regulate gene expression usually through imperfect base-pairing interactions with the 3' UTR of its target mRNAs leading to mRNA degradation and/or translational inhibition.

Lymphoid neogenesis is reported in human chronic inflammatory diseases (including SS) and associated mouse models (reviewed in [ 21, 22]).

In recent years, this hypothesis has been shown to be true with several lines of evidence from genetically modified mouse models (reviewed in 3, 32).

The role of DNA damage resulting in accelerated aging has been recapitulated in a number of mouse models (reviewed by Schumacher et al. [ 32]).

Numerous genetic mouse models used in breast cancer studies include APC, BRCA1, ERBB2 (Neu), p53, and PTEN knockout mouse models (reviewed in [ 10]).

Autophagy is impaired in the muscles of patients affected by Duchenne muscular dystrophy (DMD) and in the mdx mouse model (reviewed in De Palma et al., 2014).

Although a human segmentation molecular clock has not yet been demonstrated experimentally due to the inability to examine early developmental events in human embryos, the phenotypes associated with human vertebral malformations are very similar to the mutation phenotypes observed in mice models (reviewed in [ 83]).

In view of the important link between exercise and longevity, it is surprising that of 20 mouse models we reviewed, only two studied exercise and found it to be increased.

It thus appears that in human CCs HH-GLI signalling is operative among epithelial cells (autocrine), while the previously described paracrine signalling may reflect the nature of the mouse model used (reviewed in Theunissen & de Sauvage, 2009).

Further studies with systematic sampling and global analyses of all the available mouse models for NCLs (reviewed in [ 29]) should provide information on whether the differential expression of this gene cluster represents a hallmark of NCL diseases in general.