• In addition, we seek to understand the role of iron-sulfur cluster biogenesis in the regulation of mitochondrial iron homeostasis, and in the pathogenesis of rare diseases in which mitochondrial iron-sulfur cluster biogenesis is impaired. (nih.gov)
  • Using cell lines and tissues from patients, we are working to understand how mitochondrial iron homeostasis is regulated. (nih.gov)
  • We study mechanisms of iron sensing and control of iron homeostasis in vertebrates by iron regulated RNA binding proteins, the iron regulatory proteins (IRP). (morgridge.org)
  • IRP maintain iron homeostasis by controlling the fate of mRNA encoding proteins needed for iron metabolism or the responses to iron deficiency. (morgridge.org)
  • There are now several human disease genes that impair iron sulfur cluster biogenesis, including ISCU, frataxin, and glutaredoxin 5, LYRM4, NFU1, BOLA3, and a key feature of each disease is that mitochondrial dysfunction occurs in specific tissues and is followed by mitochondrial iron overload. (nih.gov)
  • in this case, we are using Phy-PIF optogenetics to elucidate the mechanisms by which these proteins alter mitochondrial dynamics, metabolic oscillations, and insulin secretion. (morgridge.org)