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For the mice, we proceeded with a similar analysis.
In order to identify the molecular features of the pathological programming imposed by MafB in the stem cells in Sca1-MafB mice, we proceeded initially to compare the gene expression profiles of plasma cells (B220lowCD138hiFSChiSSChi) of Sca1-MafB mice versus those from WT mice using cDNA microarray analysis.
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Since we did not detect any apoptosis-inducing properties of either the bacterially produced GST-IL-24 or the commercially available IL-24 (from mouse cells), we proceeded to produce FLAG-tagged IL-24 from supernatants of transfected Hek cells (Hek-IL-24) as has been described before (Fig. 8A) [7].
In contrast to Balb/c mice, C57BL/6 mice proceeded to lung fibrosis development following bleomycin, but not saline.
Satisfied that murine APP with the Swedish mutations would enhance the production of Aβ1-40/42, we proceeded to generate transgenic mice expressing mutant murine APP695.
After we characterized histologically the adult transgenic mice and demonstrated no differences in 3 months of age, we proceeded with the analysis of cardiovascular function.
We proceeded to assess auditory function in Tgif mutant mice.
We proceeded to investigate the cochlear phenotype of gelsolin mutant mice focusing on the development of the stereocilia bundle.
We proceeded to further characterize the responses of bak-null mice to H. felis infection.
We proceeded with analysis of cells from systemically αT2ib transduced mice.
We proceeded to explore the function of gelsolin in stereocilia by analyzing the gelsolin knockout mouse [15].
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