The haemochromatosis protein HFE induces an apparent iron-deficient phenotype in H1299 cells that is not corrected by co-expression of beta 2-microglobulin.

@article{Wang2003TheHP,
  title={The haemochromatosis protein HFE induces an apparent iron-deficient phenotype in H1299 cells that is not corrected by co-expression of beta 2-microglobulin.},
  author={Jian Wang and Guohua Chen and Kostas Pantopoulos},
  journal={The Biochemical journal},
  year={2003},
  volume={370 Pt 3},
  pages={891-9}
}
HFE, an atypical MHC class I type molecule, has a critical, yet still elusive function in the regulation of systemic iron metabolism. HFE mutations are linked to hereditary haemochromatosis type 1, a common autosomal recessive disorder of iron overload. Most patients are homozygous for a C282Y point mutation that abrogates the interaction of HFE with beta(2)-microglobulin (beta(2)M) and, thus, impairs its proper processing and expression on the cell surface. An H63D substitution is also… CONTINUE READING

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