IndraLab

Statements


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"In search of underlying molecular mechanisms, we find that CYLD knockout mice display marked overactivation of Akt and mTOR and reduced autophagic flux, and conversely, CYLD overexpression potently suppresses Akt and mTOR activity and promotes autophagy."

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"As the aforementioned results suggested that NAC could inhibit the generation of ROS in HPCCs, it is possible that mTOR, ULK1, AKT, 4E-BP1 and CYLD participate in wogonin induced autophagy, acting as upstream signals of autophagy."

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"The K63 deubiquitinase CYLD modulates autism-like behaviors and hippocampal plasticity by regulating autophagy and mTOR signaling."

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"By providing evidence that CYLD can modulate mechanistic target of rapamycin (mTOR) signaling and autophagy at the synapse, we propose that synaptic K63-linked ubiquitination processes could be fundamental in understanding the pathomechanisms underlying autism spectrum disorder."