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By using genetic knockout (WT vs. ARKO bone marrow-MSCs, BM-MSCs) or AR siRNA knockdown approach in Pten+/− PrSCs to disrupt AR expression (Supporting Information Fig S5A), we did not see ablation of AR could reverse these MSC marker expressions (Supporting Information Fig S5B D).
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The article first presents analytical expressions supported by Matlab simulation results which highlight the performance drawbacks of biased protocols such as 802.11e.
Tex19 and Sectm1 co-evolution and anti-regulated expressions support a strong functional relationship between both genes.
Interestingly, silencing ROR1 leads to an increase in Wnt5a and ROR2 expression, supporting a more invasive phenotype of melanoma cells.
TERT promoter mutations are shown to correlate with elevated mRNA expression, supporting a role in telomerase reactivation.
We detected differential CD9 methylation in 450K methylation array analyses of primary neuroblastomas, and CD9 hypermethylation was associated with reduced CD9 expression, supporting epigenetic regulation.
The proliferative activity, measured as Ki67 labeling index, showed a fourfold increase in the carcinoma cells with lost CEACAM1 expression, supporting previous observations that CEACAM1 regulates cell proliferation.
When we treated the AML cell line (M091) with decitabine, we identified ∼700 transcripts with modulated expression (Supporting Information S1).
Lactating transgenic mice exhibited strong PDK1 expression (Supporting information, Figure S1B), but no delay in involution vs. wild-type littermates (Supporting information, Figure S1C).
Similar changes were observed in IL‐11 expression (Supporting Information Fig. 1F).
Other putative Th17 markers were not associated with CD146 expression (Supporting information, Fig. S2).
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