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We emphasize that the molecular changes we observe are neither risk factors nor causes of MD.
In addition to the measurement of morphologic and molecular changes, we examined tumor-induced senescent T cells for a permanent functional alteration.
To further characterize the consequences of these molecular changes, we performed histological analysis of zona pellucida binding protein 1 (ZPBP1) and transition protein 2 (TNP2).
To understand the mechanism by which G2.2 might induce these molecular changes, we examined expression of above CSC markers at mRNA and protein levels at various time points.
Thus, the molecular changes we observed were not necessarily reflective of measurable performance changes in the parent population; see also [ 35] for related discussion.
It is not clear if the molecular changes we observe after retrieval correspond to reconsolidation or extinction of the memory trace.
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To validate whether PR cells have EMT molecular marker changes, we compared the expression of EMT markers in paired parental and resistant cell lines by RT PCR and western blotting analysis, respectively.
However, we cannot exclude the possibility that the lesions represent subclones from a precursor clone having some initial molecular change, which we did not examine.
To identify early molecular changes in AD, we used RNA-seq to generate transcriptional profiles from 22 female mice (15 AD and 7 WT) from 4, 5, and 6 months of age (see Methods).
To understand the molecular changes underlying this process, we performed proteomic and RNA array analysis.
By studying these molecular changes and their versatility, we can identify targets for sophisticated therapeutics approaches.
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