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Only CD44+ cells expressed the pluripotency genes POU5F1, NANOG and SOX2 [27], [28], [29], [29], while these markers were lost in CD44− cells, suggesting that EMT may be involved in maintaining stemness.
When grown at low (clonal) density and switched into conditions that support differentiation, the precursor markers were lost and the cells acquired morphologies and antigen expression patterns found in neurons, astrocytes, and oligodendrocytes (Figure 1G H; Table 1).
In THAL, multiple astrocytic markers were lost consistent with glial cell loss.
After differentiation into glial lineage, neuronal markers were lost, while cells that differentiated into neuronal lineage, lost glial markers [ 5, 6].
However, it is significant that all studied homing markers were lost in time following in-vitro differentiation to MoDC and that similar loss of homing markers has been described in cultured blood DC 16.
For the next round of shuffling, hybrids that were selected for ethanol tolerance (see further) or unselected hybrids were re-streaked on YPD until both markers were lost, plasmids were re-transformed, and sporulation and pairwise matings were carried out similarly as described above.
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When a dominant-negative form of lhx1 is expressed in the anterior kidney field, expression of proximal tubule markers is lost [30].
GS cannot currently account for this scenario; thus, informative markers are lost.
Expression patterns of epidermal progeny markers are lost in a ventral-to-dorsal, anterior-to-posterior manner.
Sorting procedures might be different in cultured cells as compared to uncultured cells, because expression of certain cell membrane markers is lost upon culturing.
During these cellular changes, the actin molecular architecture is disrupted and protein complexes like the cadherin catenin complex and epithelial markers are lost [ 47].
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