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In this study, we tested the therapeutic potential of mIGF-1 in the skin by generating a transgenic mouse model in which mIGF-1 expression is driven by the keratin 14 promoter.
Furthermore, our finding opens the way to the construction of a mouse model for the assessment of trogocytosis in vivo by generating a transgenic mouse expressing a selectively transferred fluorescent protein under control of an appropriate promoter driving high levels of expression on professional APCs.
We tested the hypothesis that the overexpression of PKD1L2 found in ostes/ ostes mice causes neuromuscular dysfunction in these mice by generating a transgenic mouse overexpressing PKD1L2.
By generating a transgenic zebrafish model and utilizing RNA-sequencing technology, we have examined the transcriptome of zebrafish liver tumors driven by the oncogene Myc.
In order to expand the number of BP cells in the developing mouse cerebral cortex, we began by generating a transgenic line where 4D could be overexpressed in cortical progenitors with reliable temporal control.
DOI: http://dx.doi.org/10.7554/eLife.01832.008 We confirmed these results genetically by generating a transgenic zebrafish line that drives human dominant-negative ErbB4 (DNErbB4) in neural crest-derived tissues, including Schwann cells, using the sox10 promoter.
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A study by the NIH found that generating a transgenic mouse typically takes about one year and costs between one and two hundred thousand dollars [38].
We modeled the NPARM case in vivo by generating a cognate conditional transgenic mouse line.
We generated a transgenic construct by placing Smad7 under the transcriptional control of CC10 promoter (CC10-Smad7) to express Smad7 specifically in Clara cells, which are postulated to be pivotal in forming the cell lineage of the bronchiolar epithelium [18].
To address this hypothesis without the technical limitations imposed by the transient transfection procedure, we generated a transgenic SKNBE2 cell line permanently transfected with 51A expression plasmid (hereafter referred to as SKNBE2-51A).
Although much of our studies focused on mutant LRRK2, we sought to determine if tau could be a substrate of LRRK2 in vivo by generating novel transgenic mice, which expressed human WT LRRK2 and mutant tau.
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