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Proposed model for the role of MerTK in HCC tumorigenesis. N-glycosylation modification stabilizes MerTK that promotes HCC cell growth through facilitating the Warburg effect and activating Akt/GSK3β signaling. Glucose starvation or blockade of glycosylation leads to vast non-glycosylated MerTK translocated into the nucleus, therefore promoting HCC cell survival under stress.
