BRD4-mediated ER membrane contact creates functionally distinct mitochondrial subtypes - PubMed
7 days ago
- #cellular metabolism
- #ER-mitochondria contact sites
- #BRD4
- BRD4-mediated ER membrane contact creates functionally distinct mitochondrial subtypes.
- Fedratinib, an FDA-approved drug, increases ER-mitochondria contact sites (ERMCSs) by inhibiting BRD4.
- Fedratinib reversibly alters mitochondrial and ER morphology and metabolic homeostasis.
- ERMCS modulation depends on mitochondrial electron transport chain complex III function.
- The study identifies a novel epigenetic signaling pathway linking ERMCSs and cellular metabolism.