Publications by authors named "Myagmar Tumenjargal"
Article Synopsis
- Mitochondria are crucial for non-shivering thermogenesis in brown and subcutaneous white adipose tissues (BAT and scWAT), but the specific mechanisms regulating mitochondrial function in these areas are still not fully understood.
- The study shows that prolonged β-adrenergic signaling leads to epigenetic changes in scWAT that enhance mitochondrial function through the action of a histone demethylase called JMJD1A.
- Disrupting JMJD1A in mice hampers mitochondrial biogenesis in scWAT, resulting in decreased energy expenditure and increased risks for obesity and metabolic disorders, while its role is less critical in BAT during cold stress.
Protein kinase A promotes beige adipogenesis downstream from β-adrenergic receptor signaling by phosphorylating proteins, including histone H3 lysine 9 (H3K9) demethylase JMJD1A. To ensure homeostasis, this process needs to be reversible however, this step is not well understood. We show that myosin phosphatase target subunit 1- protein phosphatase 1β (MYPT1-PP1β) phosphatase activity is inhibited via PKA-dependent phosphorylation, which increases phosphorylated JMJD1A and beige adipogenesis.
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