Kei Sakamoto

This study shows that GPCRs regulate mTORC1 substrates differently, with M5R promoting protein synthesis while allowing lysosome biogenesis.

This study identifies an autoinhibitory mechanism in the N-terminal extension of AMPKγ3 that regulates basal activity in skeletal muscle, offering a target for T2DM therapies.

The paper identifies an IL-6-associated SAA axis linked to muscle wasting and poor survival in cancer cachexia through plasma proteomics and functional studies.

This study shows that AMPK senses NAD levels, with NAD binding to the gamma subunit and modulating AMPK activity, which affects metabolic pathways like mTORC1 and autophagy.

This study shows LUBAC activates AMPK and OTULIN restricts it, affecting metabolic responses to energy stress in cells, mice, and flies.

This study shows that activating AMPK reduces excessive mitophagy and restores mitochondrial function in FBXL4-related mitochondrial DNA depletion syndrome models.

This study identifies distinct roles of AMPKγ isoforms in glucose uptake in skeletal muscle, showing γ1 is required for ADaM site activator-stimulated uptake but not AMP-binding activators.

This paper describes the mechanism and cellular effects of the potent AMPK inhibitor BAY-3827, showing it selectively blocks AMPK-dependent functions.

The paper uses proteomics to identify personalized signatures of insulin resistance and type 2 diabetes, showing that fasting proteome and phosphoproteome predict insulin sensitivity and reveal sex-specific differences.

This paper describes a protocol for analyzing muscle fiber type and cross-sectional area in cryosections of whole lower mouse hindlimbs using immunofluorescence and histochemistry.

The paper shows that AMPK activation leads to dephosphorylation of TFEB's C-terminal sites, promoting its transcriptional activation, and that AMPK is not required for mTORC1-mediated TFEB activation.

This study identifies miR-125b-5p as a glucose-regulated miRNA that negatively regulates β-cell function by modulating organelle dynamics and insulin secretion.

The paper identifies the AMPK-TFEB-FLCN axis as a regulator of cellular and metabolic homeostasis through gene expression and functional studies in mice and zebrafish.