iron transport

iron transport

the process whereby iron is carried from the intestinal mucosa to sites of use and storage. Iron binds with transferrin and shuttles to storage and utilization sites. Transferrin becomes attached to exogenous iron that enters through the intestinal villi or that reenters the plasma from the sinusoids of the spleen. The iron is then released to the normoblasts, and the transferrin is freed for additional transport functions that may involve iron stored as ferritin or hemosiderin. See also hemochromatosis, iron metabolism, transferrin.
References in periodicals archive ?
Iron transport proteins are important in particular to the hippocampal neurons, which play a large role in learning and memory.
Hepcidin Suppresses Brain Iron Accumulation by Downregulating Iron Transport Proteins in Iron-Overloaded Rats.
In future, more studies could be done to gain a better understanding of iron transport across the blood-nerve barrier, on the role of Schwann cells in regulating axon iron uptake, and on how iron participates in myelin synthesis.
2013) Adaptation of iron transport and metabolism to acute high-altitude hypoxia in mountaineers.
Intracellular iron transport and storage: from molecular mechanisms to health implications.
Hepcidin, a small antimicrobial peptide synthesized by the liver, is the principal effector of the modulation of iron metabolism, via its ability to bind ferroportin-1 (Fp-1) on cellular surface blocking its iron transport activity, and to increase Fp-1 degradation.
The challenge is to detect patients with subclinical or latent iron deficiency, without anaemia (stage 1, where stores are depleted, and stage 2, where iron transport for erythropoiesis is decreased).
Part: Brake linings, brake drums and brake shoes iron transport.
Examples of specific topics include the pharmacology of iron transport, the impact of soluble epoxide hydrolase and epoxyeicosanoids on human health, small molecule-based approaches to adult stem cell therapies, and unnatural amino acids as probes of ligand-receptor interactions and their conformational consequences.
However, these early studies are still useful in their descriptions of the generalities of iron transport, such as the energy and temperature dependence of the transport, but are not useful in the determination of the specificity of the permeases.
Since both a deficiency and an excess of iron can negatively impact brain function, the body's regulation of iron transport to the brain is crucial.
Children with a mutation in the TMPRSS6 gene produce too much hepcidin, a protein that regulates intracellular iron transport.