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Gyorgy Hajnoczky, MD, PhD

Contact Dr. Hajnoczky

1020 Locust Street
Alumni Hall, Room 527
Philadelphia, PA 19107

(215) 503-1427

Most Recent Peer-reviewed Publications

  1. Molecular mechanisms of cell death: Recommendations of the Nomenclature Committee on Cell Death 2018
  2. Endoplasmic Reticular–Mitochondrial Contactology: Structure and Signaling Functions
  3. ROS Control Mitochondrial Motility through p38 and the Motor Adaptor Miro/Trak
  4. Mitochondrial Nanotunnels
  5. Recessive mutations in MSTO1 cause mitochondrial dynamics impairment, leading to myopathy and ataxia
  6. MSTO1 is a cytoplasmic pro-mitochondrial fusion protein, whose mutation induces myopathy and ataxia in humans
  7. Intracellular Ca2+Sensing: Its Role in Calcium Homeostasis and Signaling
  8. Tissue-Specific Mitochondrial Decoding of Cytoplasmic Ca2+ Signals Is Controlled by the Stoichiometry of MICU1/2 and MCU
  9. Natural and induced mitochondrial phosphate carrier loss: Differential dependence of mitochondrial metabolism and dynamics and cell survival on the extent of depletion
  10. VDAC2-specific cellular functions and the underlying structure
  11. Subcellular ROS imaging methods: Relevance for the study of calcium signaling
  12. Redox Nanodomains Are Induced by and Control Calcium Signaling at the ER-Mitochondrial Interface
  13. MICU1 regulation of mitochondrial Ca 2+ uptake dictates survival and tissue regeneration
  14. Motifs of VDAC2 required for mitochondrial Bak import and tBid-induced apoptosis
  15. The mitochondrial phosphate carrier: Role in oxidative metabolism, calcium handling and mitochondrial disease
  16. Trans-mitochondrial coordination of cristae at regulated membrane junctions
  17. Mitochondrial ca2+uptake by the voltage-dependent anion channel 2 regulates cardiac rhythmicity
  18. Erratum: MCUR1 is an essential component of mitochondrial Ca2+uptake that regulates cellular metabolism (Nat. Cell Biol. 14, 2012 (1336-1343))
  19. Essential versus accessory aspects of cell death: Recommendations of the NCCD 2015
  20. Loss of Miro1-directed mitochondrial movement results in a novel murine model for neuron disease