Gretchen A. Meyer

This study shows that sustained Pptc7 loss in adult mice causes skeletal muscle dysfunction and reduced body mass through BNIP3 dysregulation, with partial rescue by Bnip3 KO.

The paper identifies a catecholamine-independent lipolysis pathway activated by hypoglycemia and hypoinsulinemia that enables catabolism of stable adipose tissues.

The study shows that mitochondrial function and oxidative metabolism markers in female mouse skeletal muscle lack intrinsic circadian regulation, despite core-clock genes showing rhythmicity.

This study shows that the lysosomal LRRC8 complex regulates lysosomal pH, morphology, and systemic glucose metabolism by affecting mTOR signaling and autophagic flux.

This study shows that Site-1 Protease (S1P) negatively regulates sarcolipin expression by inhibiting its promoter activity through ATF6 and CREB binding.

This study shows that loss of p300 and CBP in skeletal muscle causes severe contractile dysfunction, but mitochondrial function and cross-bridge cycling are not the primary causes.

This study identifies Site-1 Protease (S1P) as a negative regulator of muscle mass and mitochondrial metabolism by controlling the TGF-β target gene MSS51.