For this reason, we decided to utilize a mouse cell line for our studies and to prepare mutations in ank in the context of the mouse cDNA sequence.
For these experiments, we utilized a mouse mammary cancer cell line, EMT6, in which we found robust expression of the endogenous Atf3 gene in preliminary experiments.
Therefore, to directly implicate epithelial proliferative status as a contributing host factor in promoting cell fusion, we utilized a mouse model in which we could temporally manipulate epithelial proliferation in the intestine.
In this study, we utilized a mouse experimental model of peritoneal sclerosis induced by repeated injections of gastric cancer cell SF-CM.
To this end, we utilized a transgenic mouse cell line containing the JCV early promoter expressing the early genome.
In conclusion, we have investigated the imatinib and everolimus combination effect against human Ph+ quiescent leukemic cells utilizing a mouse model.
To identify novel regulators of mammary epithelial stem and progenitor cells, we utilized a GIPZ mouse transcription factor gene shRNA library to perform a screen largely based on proliferation/survival potential using primary mammary epithelial cells.
To this end we utilized 728 cells, a mouse squamous cell line derived from an EphA1/EphA2 double knockout mouse (see Methods).
To identify mitral/tufted cells in the dissociated OB culture, we utilized a transgenic mouse strain in which the endogenous neurotensin locus was replaced by neurotensin-IRES-GFP (NT-GFP) which labeled mitral and tufted cells in the OB [25].
To selectively ablate Tcf7l2 overexpression in beta cells, we utilized an inducible beta cell-specific mouse insulin promoter-1 CreER (MIP-CreER) allele, previously described (24).
To evaluate the effects of IFN-γ on osteoclastogenesis, we utilized the mouse macrophage cell line RAW264.7 (RAW cells) or splenic macrophages from CBA/BL6 mice as osteoclast precursors.
