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Article: Regulation of transferrin function and expression: Review and update

TitleRegulation of transferrin function and expression: Review and update
Authors
Issue Date1998
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/NSG
Citation
Biological Signals And Receptors, 1998, v. 7 n. 3, p. 157-178 How to Cite?
AbstractThe cellular iron uptake is a precisely controlled process to fulfill the iron demand for the synthesis and functions of a variety of iron-containing proteins, and one of the main molecules involved is the transferrin receptor (TfR), which mediates the uptake process via the transferrin cycle. The TfR expression is tightly regulated by factors such as intracellular iron level, cell proliferation or erythropoiesis at levels of receptor recycling, transcriptional or posttranscriptional control. The iron-regulatory protein/iron-responsive element system has been widely used to explain changes in receptor expression during iron loading or depletion, oxidative stress and nitric oxide stimulation. On the other hand, transcriptional control of TfR expression appears to be more important in erythroid differentiation and general cell proliferation. There is also an increasing awareness of the clinical application and experimental therapeutics based on the TfR functioning and expression. In this review, we attempt to provide a concise account of the studies of TfR structure and function as well as those areas that have not been reviewed in depth, in particular, tissue-specific regulation of TfR, the molecular mechanisms of TfR expression, and the use of TfR as diagnostic and therapeutic tools. The regulation of TfR expression in various tissues is related to its specific cellular iron requirements, Hemoglobin-synthesizing cells exhibit distinct features of iron metabolism and TfR expression as compared to most non-erythroid cells which synthesize a much lower amount of heme. For most non-erythroid cells, iron can regulate the TfR expression in a reciprocal manner through modulating the stability of the receptor mRNA whereas in hemoglobin-synthesizing cells, the TfR expression is independent of the cellular iron loading. In spite of a wide heterogeneity in the way receptor redistribution is in response to various stimuli, regulation of the constitutive expression of TfR is one of the ways of regulating the cellular iron uptake. This expression operates on both transcriptional and posttranscriptional levels. In general, factors related to cell grow th and differentiation operate on the gene transcription level, whereas iron regulates the fate of the mature mRNA.
Persistent Identifierhttp://hdl.handle.net/10722/167584
ISSN
2003 Impact Factor: 3.5

 

DC FieldValueLanguage
dc.contributor.authorLok, CNen_US
dc.contributor.authorLoh, TTen_US
dc.date.accessioned2012-10-08T03:08:47Z-
dc.date.available2012-10-08T03:08:47Z-
dc.date.issued1998en_US
dc.identifier.citationBiological Signals And Receptors, 1998, v. 7 n. 3, p. 157-178en_US
dc.identifier.issn1422-4933en_US
dc.identifier.urihttp://hdl.handle.net/10722/167584-
dc.description.abstractThe cellular iron uptake is a precisely controlled process to fulfill the iron demand for the synthesis and functions of a variety of iron-containing proteins, and one of the main molecules involved is the transferrin receptor (TfR), which mediates the uptake process via the transferrin cycle. The TfR expression is tightly regulated by factors such as intracellular iron level, cell proliferation or erythropoiesis at levels of receptor recycling, transcriptional or posttranscriptional control. The iron-regulatory protein/iron-responsive element system has been widely used to explain changes in receptor expression during iron loading or depletion, oxidative stress and nitric oxide stimulation. On the other hand, transcriptional control of TfR expression appears to be more important in erythroid differentiation and general cell proliferation. There is also an increasing awareness of the clinical application and experimental therapeutics based on the TfR functioning and expression. In this review, we attempt to provide a concise account of the studies of TfR structure and function as well as those areas that have not been reviewed in depth, in particular, tissue-specific regulation of TfR, the molecular mechanisms of TfR expression, and the use of TfR as diagnostic and therapeutic tools. The regulation of TfR expression in various tissues is related to its specific cellular iron requirements, Hemoglobin-synthesizing cells exhibit distinct features of iron metabolism and TfR expression as compared to most non-erythroid cells which synthesize a much lower amount of heme. For most non-erythroid cells, iron can regulate the TfR expression in a reciprocal manner through modulating the stability of the receptor mRNA whereas in hemoglobin-synthesizing cells, the TfR expression is independent of the cellular iron loading. In spite of a wide heterogeneity in the way receptor redistribution is in response to various stimuli, regulation of the constitutive expression of TfR is one of the ways of regulating the cellular iron uptake. This expression operates on both transcriptional and posttranscriptional levels. In general, factors related to cell grow th and differentiation operate on the gene transcription level, whereas iron regulates the fate of the mature mRNA.en_US
dc.languageengen_US
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/NSGen_US
dc.relation.ispartofBiological Signals and Receptorsen_US
dc.subject.meshBase Sequenceen_US
dc.subject.meshBiological Transporten_US
dc.subject.meshErythropoiesisen_US
dc.subject.meshGene Expression Regulationen_US
dc.subject.meshIron - Metabolismen_US
dc.subject.meshMolecular Sequence Dataen_US
dc.subject.meshReceptors, Transferrin - Physiologyen_US
dc.subject.meshTissue Distributionen_US
dc.subject.meshTransferrin - Physiologyen_US
dc.titleRegulation of transferrin function and expression: Review and updateen_US
dc.typeArticleen_US
dc.identifier.emailLok, CN:cnlok@hku.hken_US
dc.identifier.authorityLok, CN=rp00752en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1159/000014542-
dc.identifier.pmid9672759-
dc.identifier.scopuseid_2-s2.0-0031833094en_US
dc.identifier.volume7en_US
dc.identifier.issue3en_US
dc.identifier.spage157en_US
dc.identifier.epage178en_US
dc.publisher.placeSwitzerlanden_US
dc.identifier.scopusauthoridLok, CN=7006410829en_US
dc.identifier.scopusauthoridLoh, TT=7102125300en_US

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