Sentence examples for mouse models confirming from inspiring English sources

The activation of β-catenin introduced by stabilizing mutations and nonsense mutations in APC produce similar but not identical cancers in mouse models, confirming that some β-catenin-independent functions for APC can contribute to tumorigenesis (Harada et al., 1999).

Mouse models confirm that intestinal barrier dysregulation alone is insufficient to cause disease, but they also show that enhanced tight junction permeability can accelerate disease onset and increase severity.

Our initial findings of distribution of 89Zr-labeled hMSCs in mouse models confirm the biostability of the radiolabel bound to the DFO moiety supporting further exploration of the 89Zr-DBN labeling method for monitoring stem cell engraftment and cell trafficking.

Conditional Pten knockout mouse models confirmed that Pten inactivation plays an important role in cancer development and tumor progression.

Albeit our results obtained in two genetically modified mouse models confirm that an antagonism of Wnt signaling in osteoblasts has a negative effect on bone formation, they were not necessarily expected, based on several findings published by others.

Experimental studies using mouse models confirm that genetic and chemical ablation of macrophages leads to an inhibition of tumor progression and reduced rate of metastasis [8], [9], [10], [11].

Mouse models confirm that relatively modest changes in Grem1 expression influence intestinal tumor burden, possibly through variation in apoptosis.

Studies in Actn4 KO, Actn4 KI, and transgenic Actn4 mouse models confirm the importance of this gene in kidney function.

Mouse models confirmed that connexin26 and connexin30 are essential for auditory function, as well as survival and development of the organ of Corti [ 169- 175].

The use of appropriate transgenic mouse models confirmed these findings in rodents and eventually clarified the underlying mechanism defining cyclin E1 as a promising new therapeutic target.

Inactivation of Hod in transgenic mouse models confirm that an absence of Hod results in an imbalance between proliferation and differentiation of cardiomyocytes, culminating in impaired cardiac development [ 44, 45].