Translational control of ceruloplasmin gene expression: Beyond the IRE

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...

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Autores principales:	MAZUMDER,BARSANJIT, SAMPATH,PRABHA, FOX,PAUL L
Lenguaje:	English
Publicado:	Sociedad de Biología de Chile 2006
Materias:	Translational control ceruloplasmin iron homeostasis GAIT element inflammation
Acceso en línea:	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602006000100007
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spelling	oai:scielo:S0716-976020060001000072006-06-30Translational control of ceruloplasmin gene expression: Beyond the IREMAZUMDER,BARSANJITSAMPATH,PRABHAFOX,PAUL L Translational control ceruloplasmin iron homeostasis GAIT element inflammation 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)-γ 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.info:eu-repo/semantics/openAccessSociedad de Biología de ChileBiological Research v.39 n.1 20062006-01-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602006000100007en10.4067/S0716-97602006000100007
institution	Scielo Chile
collection	Scielo Chile
language	English
topic	Translational control ceruloplasmin iron homeostasis GAIT element inflammation
spellingShingle	Translational control ceruloplasmin iron homeostasis GAIT element inflammation MAZUMDER,BARSANJIT SAMPATH,PRABHA FOX,PAUL L Translational control of ceruloplasmin gene expression: Beyond the IRE
description	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)-γ 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.
author	MAZUMDER,BARSANJIT SAMPATH,PRABHA FOX,PAUL L
author_facet	MAZUMDER,BARSANJIT SAMPATH,PRABHA FOX,PAUL L
author_sort	MAZUMDER,BARSANJIT
title	Translational control of ceruloplasmin gene expression: Beyond the IRE
title_short	Translational control of ceruloplasmin gene expression: Beyond the IRE
title_full	Translational control of ceruloplasmin gene expression: Beyond the IRE
title_fullStr	Translational control of ceruloplasmin gene expression: Beyond the IRE
title_full_unstemmed	Translational control of ceruloplasmin gene expression: Beyond the IRE
title_sort	translational control of ceruloplasmin gene expression: beyond the ire
publisher	Sociedad de Biología de Chile
publishDate	2006
url	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602006000100007
work_keys_str_mv	AT mazumderbarsanjit translationalcontrolofceruloplasmingeneexpressionbeyondtheire AT sampathprabha translationalcontrolofceruloplasmingeneexpressionbeyondtheire AT foxpaull translationalcontrolofceruloplasmingeneexpressionbeyondtheire
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Translational control of ceruloplasmin gene expression: Beyond the IRE

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