Fig. 7: A mechanism underlying GFAT1-drived cancer cell survival under glucose starvation.

A schematic model showing the molecular basis of GFAT1-TAB1-p38 signaling in autophagy-induced cancer cell survival. Glucose deficiency promotes TAB1 S438 phosphorylation by JNK/p38 MAPK and subsequent TTLL5–GFAT1–TAB1 complex formation. GFAT1-derived glutamate facilitates TAB1 E212 glutamylation through TTLL5, resulting in enhanced TAB1-p38 MAPK interaction and p38 MAPK autophosphorylation. GFAT1-TAB1-p38 MAPK axis sustains cancer cell survival under glucose deprivation via autophagy.