Iron Transport
symposium 342 Harris/Gitlin Doug Templeton
doug.templeton@utoronto.ca
Hi Leah. I have been thinking along the lines that in the absence of ferroxidase activity, Fe3+ was not being made available to transferrin and non-transferrin-bound Fe was deposited in soft tissues instead. You seem to imply here that ceruloplasmin is needed for efflux of Fe, and Fe accumulation in aceruloplasminemia is a defect in efflux. I suppose if efflux is linked to acquisition by Tf this could be the same thing. As you know, Young et al. showed in FEBS Lett. 1997 that Cp increased Fe efflux from HepG2 cells, but Paul Fox in Science this year had a somewhat different result (and see paper 706 in this symposium).Doug Templeton
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Thu Dec 10