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By using the SDIA method, we induced dopaminergic (DA) neurons by coculturing HLA-G1-H1 hES cells with the mouse stromal cell line PA6.
We also demonstrated the applicability of these assays for species-specific quantitation of transcriptional expression of mouse stromal cell genes including Dpp4, Dpp8, Dpp9, Fap and Cxcr4 in mixed human-mouse RNA samples from human glioma cell-derived tumor xenografts growing in mouse brain.
DA neuron induction can be achieved by co-culturing ESC with the mouse stromal cell lines PA6 or MS5.
HOZOTs were purified by Ficoll-Paque to deplete debris from mouse stromal cell lines killed by HOZOTs before experiments.
Dopaminergic differentiation of BG03 was induced by co-culture with the mouse stromal cell line PA6 as described previously [9].
Investigators have demonstrated the expression of introduced TCRs following differentiation of human progenitor cells on mouse stromal cell lines expressing the Delta-like 1 molecule [15], [16].
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In addition, unlike the mouse epithelium, which does not proliferate or show regulation of PR expression in response to E2 in association with uterine stroma derived from mice that are null for the AF-1 domain of ERα, hUtE proliferates and PR are up-regulated in response to E2 in association genetically identical ERα knock-out mouse stromal cells.
Tumor cells from the blood of the patient GEN were seeded on irradiated adherent mouse stromal cells (MS-5) in 10% FCS complete RPMI medium, without any cytokine.
Clones were expanded and analyzed for human-specific and cancer markers (to exclude the presence of mouse stromal cells) as well as epithelial and mesenchymal markers (Figure 1C).
Alternatively, it is possible that the anti-Myc antibody might cross-react to some degree with mouse stromal cells as some cross reactivity with mouse Myc has been reported for the 9E10 mAb [48].
Thus, while this data does not exclude a significant contribution from mouse stromal cells infiltrating the tumor to the resistance mechanism, it does suggest that any stromal changes may be driven, at least in part, by treatment induced changes in the tumor cells.
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