Molecular basis of hereditary iron homeostasis defects
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61989592%3A15110%2F10%3A10211948" target="_blank" >RIV/61989592:15110/10:10211948 - isvavai.cz</a>
Result on the web
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DOI - Digital Object Identifier
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Alternative languages
Result language
angličtina
Original language name
Molecular basis of hereditary iron homeostasis defects
Original language description
Iron is a trace element that is vital for life. It is a component of innumerable hemoproteins and many essential non-heme iron proteins that are involved in oxygen binding and metabolism and electron transfer. Nevertheless, iron can also be toxic to cells as it catalyses the production of oxygen radicals. Iron uptake, transport, storage and utilization are therefore strictly regulated to meet the body's iron needs and to avoid its potential toxicity. Any imbalance in iron homeostasis may lead to the development of pathological conditions associated with either iron overload or iron deficiency. In this paper, we review the current understanding of iron biology with a focus on erythroid iron demand. In addition, we will discuss molecular pathophysiologywith implications for novel therapies of selected hereditary defects of iron homeostasis.
Czech name
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Czech description
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Classification
Type
J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)
CEP classification
FD - Oncology and haematology
OECD FORD branch
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Result continuities
Project
Result was created during the realization of more than one project. More information in the Projects tab.
Continuities
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)<br>Z - Vyzkumny zamer (s odkazem do CEZ)
Others
Publication year
2010
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Hematology
ISSN
1024-5332
e-ISSN
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Volume of the periodical
15
Issue of the periodical within the volume
2
Country of publishing house
GB - UNITED KINGDOM
Number of pages
6
Pages from-to
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UT code for WoS article
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EID of the result in the Scopus database
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