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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].
Sorting procedures might be different in cultured cells as compared to uncultured cells, because expression of certain cell membrane markers is lost upon culturing.
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No additional markers were lost on longer-term follow-up.
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).
GS cannot currently account for this scenario; thus, informative markers are lost.
In THAL, multiple astrocytic markers were lost consistent with glial cell loss.
Expression patterns of epidermal progeny markers are lost in a ventral-to-dorsal, anterior-to-posterior manner.
After differentiation into glial lineage, neuronal markers were lost, while cells that differentiated into neuronal lineage, lost glial markers [ 5, 6].
During these cellular changes, the actin molecular architecture is disrupted and protein complexes like the cadherin catenin complex and epithelial markers are lost [ 47].
However, with continued passaging of ASCs, these APC-associated markers are lost, effectively mitigating the immune response until it has been eliminated.
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