Figure 7.

Model for the GRK2-dependent activation of the HuR/HIF1α axis. In basal conditions, the main HuR protein pool is located in the nucleus. Hypoxia or adrenergic signaling facilitates GRK2 phosphorylation at Ser670, enabling HuR phosphorylation by GRK2, thus increasing HuR nuclear export. Cytosolic HuR protein binds to and stabilizes HIF1-α mRNA, increasing protein translation and HIF1-α function as a transcription factor. As a consequence, transcription and protein secretion of the VEGF-C angiogenic factor would be enhanced (scheme created with BioRender).