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Ivana De Domenico
Researcher at University of Utah
Publications - 49
Citations - 5512
Ivana De Domenico is an academic researcher from University of Utah. The author has contributed to research in topics: Ferroportin & Hepcidin. The author has an hindex of 30, co-authored 49 publications receiving 5158 citations. Previous affiliations of Ivana De Domenico include University of Messina.
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The serine protease matriptase-2 (TMPRSS6) inhibits hepcidin activation by cleaving membrane hemojuvelin.
Laura Silvestri,Alessia Pagani,Antonella Nai,Ivana De Domenico,Jerry Kaplan,Clara Camaschella +5 more
TL;DR: The inhibitory effect of matriptase-2 on hepcidin promoter is confirmed and it is shown that matript enzyme-2 lacking the serine protease domain is fully inactive and that mutant R774C found in patients with genetic iron deficiency has decreased inhibitory activity.
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Regulation of iron acquisition and storage: consequences for iron-linked disorders
TL;DR: Findings of iron transporters and insights into their regulation have provided important information about iron metabolism and genetic iron disorders.
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The molecular mechanism of hepcidin-mediated ferroportin down-regulation
Ivana De Domenico,Diane M. Ward,Charles Langelier,Michael B. Vaughn,Elizabeta Nemeth,Wesley I. Sundquist,Tomas Ganz,Giovanni Musci,Jerry Kaplan +8 more
TL;DR: Ferroportin (Fpn) is the only known iron exporter in vertebrates and it is shown that after binding of hepcidin, Fpn is tyrosine phosphorylated at the plasma membrane, and adjacent tyrosines as the phosphorylation sites are identified.
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A heme export protein is required for red blood cell differentiation and iron homeostasis
Sioban Keel,Raymond T. Doty,Zhantao Yang,John G. Quigley,Jing Chen,Sue E. Knoblaugh,Paul D. Kingsley,Ivana De Domenico,Michael B. Vaughn,Jerry Kaplan,James Palis,Janis L. Abkowitz +11 more
TL;DR: In this paper, the feline leukemia virus, subgroup C, receptor (FLVCR) exports cytoplasmic heme to macrophages that ingest senescent red cells and regulates hepatic iron.
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Ferroxidase activity is required for the stability of cell surface ferroportin in cells expressing GPI‐ceruloplasmin
Ivana De Domenico,Diane M. Ward,Maria Carmela Bonaccorsi di Patti,Suh Young Jeong,Samuel David,Giovanni Musci,Jerry Kaplan +6 more
TL;DR: The requirement for a ferroxidase to maintain iron transport activity represents a new mechanism of regulating cellular iron export, a new function for Cp and an explanation for brain iron overload in patients with aceruloplasminemia.