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Given that both mouse models shared this phenotype, we used f-FoxO1 mice for the following mechanistic study.
Comparing the gene expression profile of the NELF-B KO with previously published microarray data from PPARα KO myocardium (Georgiadi et al., 2012), we found that these two KO mouse models shared a substantial overlap in downregulated target genes (p < 1 × 10−5; Figure 3A), 85% of which are metabolism-related.
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Thus, while these two mouse models share some pathophysiological changes at the myotendinous junction, myonuclei clustering is a specific feature of lamin A/C-deficient muscles.
These findings suggest that all three mouse models share a common signaling pathway for RGC death and beyond, although the function of each protein is distinct.
Along with an invasive phenotype, the GL261 mouse model shares many histopathological markers with human GBM.
Therefore, the Eμ- HMGA2 transgenic mouse model shares the same functional attributes and molecular signature as human T-ALL.
This suggests that the 3xTg AD mouse model shares some similarities with the human AD pathology and indeed this model displays plaques as well as Tau pathology.
We report that the mouse model shares with cAMN and cALD a common signature comprising dysregulation of oxidative phosphorylation, adipocytokine and insulin signaling pathways, and protein synthesis.
Indeed, both mouse models, which shared the same mixed genetic background, were characterized by short lifespan, reduced weight gain, severe megalencephaly and ventricular enlargement, increased cortical thickness, cortical lamination defects, hippocampal alterations, hypomyelination, and spontaneous epilepsy.
These three mouse models all share a pattern of peripheral degeneration with Optn E50K mice.
Jim Olson has already begun preparing a web-based system of his laboratory's available mouse models for sharing and has volunteered to expand this effort to the global medulloblastoma community.
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