Sentence examples for mouse models confirmed from inspiring English sources
Conditional Pten knockout mouse models confirmed that Pten inactivation plays an important role in cancer development and tumor progression.
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.
Further investigation in human and mouse models confirmed that mutant SPOP blocks a process called called homology directed repair: this is the method that cells normally use to repair double-stranded DNA breaks.
Following this, studies using induced diabetes mouse models confirmed that MSC-islet co-transplantation not only reversed diabetes but also significantly increased the number of recipient islets [ 42, 43].
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.
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.
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].
