Embedded within S6K1 is a target-selective kinase phospho-code that integrates signals from mTORC1 and Cdk5 to direct an insulin-stimulated post-translational metabolon determining adipocyte lipid metabolism.
Our data demonstrated that S6K1 was the downstream effector of mTOR and that S6K1 was critical for both rod and cone survival in Retinitis pigmentosa (RP). Our findings make a strong case for targeting S6K1 as a promising therapeutic strategy for promoting the survival of photoreceptors in RP
DPP-4 inhibitor sitagliptin has effects on cardiac function glycemia and beta-cell function together with reducing S6K1 activation and IRS-1 and IRS-2 degradation in the obesity female mouse model
S6K1-dependent IRS-1pSer suppresses insulin signaling leading to insulin resistance which is frequently observed in AD brains. Notably miR-200b/c transfection of SH-SY5Y cells reduced the levels of IRS-1pSer. This finding indicates that miR-200b/c has the potential to alleviate insulin resistance via modulation of S6K1
These results suggest that S6K1 drives the alpha to beta transition through the epigenetic regulation of cell-specific genes including insulin and glucagon. This novel role of S6K1 in islet cells provides basic clues to establish therapeutic strategies against T1DM.
In high-fat fed mice loss of S6K1 mimics endurance exercise training by reducing mitochondrial ROS production and upregulating oxidative utilization of ketone bodies.
We provide mechanistic evidence that S6K1's negative feedback to PI3K signaling is involved in axon growth inhibition and show that phosphorylation of S6K1 is a more appropriate regeneration indicator than is S6 phosphorylation.
we show that simultaneous inhibition of mTOR signaling to both S6K1 and 4E-BP1 is sufficient to reduce AKT-induced muscle growth and render it insensitive to the mTORC1-inhibitor rapamycin
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