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Using a thy1-GFP morphological marker, we demonstrated that in CA1 pyramidal neurons, transgenic miR132 induces an increase in dendrite spine density.
Using immunostaining for the androgen receptor and p63, a basal epithelial cell marker, we demonstrated that the menin-negative prostate cancer cells did not display p63 expression and that the androgen receptor was expressed but more heterogeneous in these lesions.
Further, using expression of a fluorescent protein marker, we demonstrated the ability to repeatedly invert specific transcripts between an active and inactive state in an otherwise isogenic cell background.
With the use of CD68 as a macrophage marker, we demonstrated that expression levels of CD68 in EAT and MAT were significantly higher in obese CAD group compared to controls, and also MAT CD68 was significantly higher compared to EAT and SAT in obese CAD group.
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Using controlled mating experiments, assigning paternity using microsatellite markers, we demonstrated that sperm usage is highly variable in the stalk-eyed fly T. dalmanni.
By employing a suite of 20 informative nuclear SSR markers, we demonstrated the general genetic distinctiveness of R. mucronata and R. stylosa, and potential hybridization or introgression between them.
The lower level of gene and protein expression of neuronal markers we demonstrated in CNS PNETs with WNT/ β-catenin pathway activation compared with those without suggested these tumours show little neuronal differentiation supporting this hypothesis.
In order to measure more accurately the overexpression of different stem (Nestin, A2B5, Nanog and Notch1) and differentiation (GFAP) markers, we demonstrated by FACS analysis in all the cell lines that 3-Gy-irradiated cells cultured in SCM medium either markedly upregulated these stem markers or downregulated GFAP compared with the control SCM condition.
Using presence-absence molecular markers we demonstrate that single Arabidopsis plants can have multiple genotypes.
Using a subset of 10 markers, we demonstrate the utility of the developed markers in phylogenetic and evolutionary rate analyses.
In addition, combining a gene loss-of-function phenotype screen with detection of integrated fluorescent markers, we demonstrate that targeted knock-ins in Caenorhabditis elegans also can be achieved by homology-independent repair.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com