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As shown in Figure 4A, B, cotreatment of C6 cells with Ado blocked CHX-induced increase in intracellular cAMP in C6 cells and prevented CHX-promoted C6 cell phenotypic change of differentiation.
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We therefore hypothesized that the loss of H3mm7 caused the expression rate change of differentiation-related genes and thus the proportion of successfully differentiated cells decreased despite the isogenicity of the H3mm7−/− C2C12 cells.
In vitro live cell tracking to trace the dynamic changes of differentiation toward neuronal fate by miR-124a would have also inform us when we can expect the probable changes of cellular fate after in vivo administration despite the difference between in vitro and in vivo situation.
Although sampling additional populations would no doubt refine our understanding of genetic differentiation in this species, we suggest that it will not substantially change estimates of differentiation between Hawaii and Japan.
Thus, quantitative change of tumor differentiation should arise from accumulation of mutations according to the V theory of tumorigenesis [4], [5].
DLD1 cells expressing GFP-GFP-HAND1 exhibited a similar morphological change of terminal differentiation (Supplementary Figure S3).
In order to characterize the change of cell differentiation markers on THP-1 cells, we measured pDC-specific and mDC-specific markers on THP-1 cells by flow cytometry.
Furthermore, Flcn or Fnip1 overexpression did not induce transcriptional changes indicative of differentiation or accelerate ESC commitment.
Notably, HAND1-expressing DLD1 cells maintained in Dox progressively displayed morphological changes characteristic of differentiation, including giant cell phenotype, flat and elongated morphology and multinucleate formation, which was not seen in the control.
When bFGF and EGF were removed and replaced by serum, most but not all spheres underwent changes characteristic of differentiation: they adhered rapidly to the plastic substrate, the cells flattened and acquired a fusiform shape.
This effect was presumed to be a result of the loss of MafB that stimulated GATA-1 to change the direction of differentiation.
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