Zhiyun Ye

TL;DR: An AMP/ADP-independent mechanism that triggers AMPK activation by sensing the absence of fructose-1,6-bisphosphate (FBP), with AMPK being progressively activated as extracellular glucose and intracellular FBP decrease is described.

TL;DR: This study found that the late endosomal/lysosomal protein complex v-ATPase-Ragulator, essential for activation of mTORC1, is also required for AMPK activation and uncovered that AMPK is a residential protein of late endo-lysosome.

TL;DR: The octaketide cytosporone B (Csn-B) is a naturally occurring agonist for Nur77 that induced apoptosis and retarded xenograft tumor growth by inducing Nur77 expression, translocating Nur77 to mitochondria to cause cytochrome c release and may be useful as a reagent to increase understanding of Nur77 biological function.

TL;DR: It is shown that it is AMP, but not ADP, that drives AXIN to directly tether LKB1 to phosphorylate AMPK, and that AXIN directly transmits AMP binding of AMPK to its activation by L KB1, uncovering the mechanistic route for AMP to elicit AMPK activation byLKB1.

TL;DR: The results show that Axin acts as a tumor suppressor by facilitating p53 function through integration of multiple factors.