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Proposed mechanism of HULC upregulation in hepatocellular carcinoma. (1) The kinase PRKACB functions as an activator of CREB. (2) Phosphorylated (activated) CREB forms part of the RNA pol II transcriptional machinery to activate HULC expression. (3) Abundant HULC RNA acts as a molecular sponge to sequester and inactivate the repressive function miR-372. (4) PRKACB levels increase, as transcripts are normally translationally repressed by high miR-372 levels.
