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Title: Translational control of ceruloplasmin gene expression: Beyond the IRE
Authors: Mazumder, B
Sampath, P 
Fox, P.L
Keywords: ceruloplasmin
gamma interferon
gamma interferon activated inhibitor of translation
iron regulatory factor
messenger RNA
mitogen activated protein kinase
protein inhibitor
unclassified drug
3' untranslated region
5' untranslated region
conference paper
gel mobility shift assay
gene expression
gene silencing
iron deficiency anemia
iron metabolism
iron responsive element
macrophage activation
mitochondrial membrane
protein analysis
protein binding
protein function
protein phosphorylation
protein synthesis
regulatory mechanism
RNA structure
translation regulation
Issue Date: 2006
Publisher: Society of Biology of Chile
Citation: Mazumder, B, Sampath, P, Fox, P.L (2006). Translational control of ceruloplasmin gene expression: Beyond the IRE. Biological Research 39 (1) : 59-66. ScholarBank@NUS Repository.
Rights: Attribution 4.0 International
Abstract: Translational control is a common regulatory mechanism for the expression of iron-related proteins. For example, three enzymes involved in erythrocyte development are regulated by three different control mechanisms: globin synthesis is modulated by heme-regulated translational inhibitor; erythroid 5-aminolevulinate synthase translation is inhibited by binding of the iron regulatory protein to the iron response element in the 5?-untranslated region (UTR); and 15-lipoxygenase is regulated by specific proteins binding to the 3?-UTR. Ceruloplasmin (Cp) is a multi-functional, copper protein made primarily by the liver and by activated macrophages. Cp has important roles in iron homeostasis and in inflammation. Its role in iron metabolism was originally proposed because of its ferroxidase activity and because of its ability to stimulate iron loading into apo-transferrin and iron efflux from liver. We have shown that Cp mRNA is induced by interferon (IFN)-y in U937 monocytic cells, but synthesis of Cp protein is halted by translational silencing. The silencing mechanism requires binding of a cytosolic inhibitor complex, IFN-Gamma-Activated Inhibitor of Translation (GAIT), to a specific GAIT element in the Cp 3?-UTR. Here, we describe our studies that define and characterize the GAIT element and elucidate the specific trans-acting proteins that bind the GAIT element. Our experiments describe a new mechanism of translational control of an iron-related protein and may shed light on the role that macrophage-derived Cp plays at the intersection of iron homeostasis and inflammation. © 2006 Sociedad de Biología Chile.
Source Title: Biological Research
ISSN: 0716-9760
DOI: 10.4067/S0716-97602006000100007
Rights: Attribution 4.0 International
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