Fig. 9: Proposed model of LATS2 action in β-cells. | Nature Communications

Fig. 9: Proposed model of LATS2 action in β-cells.

From: The Hippo kinase LATS2 impairs pancreatic β-cell survival in diabetes through the mTORC1-autophagy axis

Fig. 9

LATS2, mTORC1, and autophagy may constitute a stress-sensitive survival pathway. Under physiological (Hippo”OFF”) or acute stress conditions, autophagy promotes β-cell survival by directly degrading LATS2 and consequently reinforcing protective-autophagy mechanism through a positive-feedback loop. However, prolonged diabetogenic stress activated LATS2 (Hippo “ON”) leading to mTORC1 hyper-activation, defective autophagy, ultimately further LATS2 accumulation and subsequent β-cell apoptosis. LATS2 (Large tumor suppressor 2; in orange), MST1/2 (Mammalian Sterile 20-like kinases 1/2; in blue), MOB1 (Mps-one binder 1; in beige), mTORC1 (Mammalian target of rapamycin complex 1; in green).

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