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A Heme Export Protein Is Required for Red Blood Cell Differentiation and Iron Homeostasis
The feline leukaemia virus subgroup C receptor (FLVCR) exports cytoplasmic heme. A lab group from the University of Washington in Seattle (USA) now demonstrates how FLVCR-null mice lack proper erythropoiesis and show craniofacial and limb deformities similar to those observed in patients with Diamond-Blackfan anemia. The animals die in midgestation.
Mice in which the FLVCR is deleted neonatally develop a severe macrocytic anemia with proerythroblast maturation arrest. It is therefore assumed that erythroid precursors export more heme to ensure survival. Haemoproteins are important for function and intactness of aerobic cells. Yet free heme is toxic, which is why cells must balance their heme synthesis.
The scientists further discovered that FLVCR regulates hepatic iron and orchestrates heme export from macrophages that absorb old red cells.
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05.05.2008 | Anna Lena Marwedel 
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