A fungal multicopper oxidase restores iron homeostasis in aceruloplasminemia.
Mutations that lead to a loss of the copper-containing plasma enzyme ceruloplasmin disrupt mammalian iron homeostasis. The mechanism by which ceruloplasmin mobilizes iron from cell stores has been controversial. We demonstrate that injection of a soluble copper-containing yeast protein Fet3p can restore iron homeostasis in phlebotomized mice with a deletion of the ceruloplasmin gene. These results show the conservation of function of copper-containing proteins in eukaryotic iron metabolism.
Harris
Z Leah
ZL
Department of Anesthesiology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Davis-Kaplan
Sandra R
SR
Gitlin
Jonathan D
JD
Kaplan
Jerry
J
D000818:Animals; D002570:Ceruloplasmin / Q000172:deficiency* / Q000235:genetics* / Q000627:therapeutic use; D005656:Fungal Proteins / Q000627:therapeutic use; D017353:Gene Deletion; D006706:Homeostasis; D007501:Iron / Q000378:metabolism*; D051379:Mice; D029701:Saccharomyces cerevisiae Proteins; D014168:Transferrin / Q000378:metabolism
D005656:Fungal Proteins; D029701:Saccharomyces cerevisiae Proteins; D014168:Transferrin; D007501:Iron; D002570:Ceruloplasmin; C085513:FET3 protein, S cerevisiae