![]() ![]() This permits expression of ARE mRNAs that promote chemoresistance. Mechanistically, we find the stress-responsive p38 MAPK-MK2 signaling pathway stabilizes ARE mRNAs by phosphorylation and inactivation of mRNA decay factor, Tristetraprolin (TTP) in G0. Importantly, AU-rich elements (AREs) are significantly enriched in the upregulated G0 translatome and transcriptome. In G0 cells, canonical translation initiation is inhibited yet we find that inflammatory genes are highly translated, indicating alternative post-transcriptional regulation. We find that our resistant G0 cells recapitulate gene expression profiles of in vivo chemoresistant leukemic and G0 models. To study post-transcriptional regulation in G0 leukemic cells, we systematically analyzed their transcriptome, translatome, and proteome. ![]() We induce chemoresistant and G0 leukemic cells by serum starvation or chemotherapy treatment.
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