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We used these techniques to probe the intrinsic mechanism of chondroid cell dedifferentiation in order to provide a feasible solution for this in cell culture.
Had tenOever not pursued the viral infection studies at Mount Sinai, he adds, "we simply wouldn't have discovered this [second] role of the kinase, because you'd never detect this in cell culture".
Importantly, using anti-ZIP6 antibodies, we have confirmed this in cell lines and clinical material [ 8].
While it appears that redistribution of intracellular Ca2+ does occur following these agents, the importance of this in cell injury is not fully resolved.
This may reflect differences in molecular compared to histological subtyping, discordance between mRNA and protein expression (although we have not observed this in cell lines, data not shown), or the quantitative limitations of array-based transcriptome analysis, emphasizing the importance of protein expression analysis.
Enter this in cell D4.
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The aim of this study is to probe the intrinsic mechanism of chondroid cell dedifferentiation in order to provide a feasible solution for this in cell culture.
This in-cell ELISA method can be used with any TRKA rearranged oncogenic fusion cell type and can be extended to other TRK isoforms as well.
Could authors test this in cells or in vitro.
The authors could not prove this in cells arrested by Vprv.
This increase in cell number is usually associated with the emergence of a "mature" zonation pattern.
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