Differential role of glutaredoxin and thioredoxin in metabolic oxidative stress-induced activation of apoptosis signal-regulating kinase 1.
Identifieur interne : 000F43 ( Main/Exploration ); précédent : 000F42; suivant : 000F44Differential role of glutaredoxin and thioredoxin in metabolic oxidative stress-induced activation of apoptosis signal-regulating kinase 1.
Auteurs : Jae J. Song [États-Unis] ; Yong J. LeeSource :
- The Biochemical journal [ 0264-6021 ] ; 2003.
Descripteurs français
- KwdFr :
- Activation enzymatique (MeSH), Adenoviridae (génétique), Buthionine sulfoximine (pharmacologie), Catalase (métabolisme), Cellules cancéreuses en culture (MeSH), Glucose (métabolisme), Glutarédoxines (MeSH), Humains (MeSH), MAP Kinase Kinase Kinase 5 (MeSH), MAP Kinase Kinase Kinases (métabolisme), Mâle (MeSH), Oxidoreductases (MeSH), Protéines (physiologie), Stress oxydatif (MeSH), Thiorédoxines (métabolisme), Vecteurs génétiques (MeSH).
- MESH :
- génétique : Adenoviridae.
- métabolisme : Catalase, Glucose, MAP Kinase Kinase Kinases, Thiorédoxines.
- pharmacologie : Buthionine sulfoximine.
- physiologie : Protéines.
- Activation enzymatique, Cellules cancéreuses en culture, Glutarédoxines, Humains, MAP Kinase Kinase Kinase 5, Mâle, Oxidoreductases, Stress oxydatif, Vecteurs génétiques.
English descriptors
- KwdEn :
- Adenoviridae (genetics), Buthionine Sulfoximine (pharmacology), Catalase (metabolism), Enzyme Activation (MeSH), Genetic Vectors (MeSH), Glucose (metabolism), Glutaredoxins (MeSH), Humans (MeSH), MAP Kinase Kinase Kinase 5 (MeSH), MAP Kinase Kinase Kinases (metabolism), Male (MeSH), Oxidative Stress (MeSH), Oxidoreductases (MeSH), Proteins (physiology), Thioredoxins (metabolism), Tumor Cells, Cultured (MeSH).
- MESH :
- chemical , metabolism : Catalase, Glucose, MAP Kinase Kinase Kinases, Thioredoxins.
- chemical , pharmacology : Buthionine Sulfoximine.
- genetics : Adenoviridae.
- chemical , physiology : Proteins.
- Enzyme Activation, Genetic Vectors, Glutaredoxins, Humans, MAP Kinase Kinase Kinase 5, Male, Oxidative Stress, Oxidoreductases, Tumor Cells, Cultured.
Abstract
Redox-sensing molecules such as thioredoxin (TRX) and glutaredoxin (GRX) bind to apoptosis signal-regulating kinase 1 (ASK1) and suppress its activation. Glucose deprivation disrupted the interaction between TRX/GRX and ASK1 and subsequently activated the ASK1-stress-activated protein kinase/extracellular-signal-regulated kinase kinase-c-Jun N-terminal kinase 1 (JNK1) signal-transduction pathway. L-Buthionine-( S, R )-sulphoximine, which decreases intracellular glutathione content, enhanced glucose deprivation-induced activation of JNK1 by promoting the dissociation of TRX, but not GRX, from ASK1. Treatment of cells with exogenous glutathione disulphide ester resulted in the dissociation of GRX, but not TRX, from ASK1 and the subsequent activation of JNK1. Nonetheless, overexpression of calatase, an H(2)O(2) scavenger, inhibited JNK1 activation and cytotoxicity as well as the dissociation of TRX and GRX from ASK1 during combined glucose deprivation and L-buthionine-( S, R )-sulphoximine treatment. Taken together, glucose deprivation-induced metabolic oxidative stress may activate ASK1 through two different pathways: glutathione-dependent GRX-ASK1 and glutathione-independent TRX-ASK1 pathways.
DOI: 10.1042/BJ20030275
PubMed: 12723971
PubMed Central: PMC1223534
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Differential role of glutaredoxin and thioredoxin in metabolic oxidative stress-induced activation of apoptosis signal-regulating kinase 1.</title><author><name sortKey="Song, Jae J" sort="Song, Jae J" uniqKey="Song J" first="Jae J" last="Song">Jae J. Song</name><affiliation wicri:level="4"><nlm:affiliation>Department of Surgery and Cancer Institute, Hillman Cancer Center, University of Pittsburgh, Pittsburgh, PA 15213, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Surgery and Cancer Institute, Hillman Cancer Center, University of Pittsburgh, Pittsburgh, PA 15213</wicri:regionArea><placeName><region type="state">Pennsylvanie</region><settlement type="city">Pittsburgh</settlement></placeName><orgName type="university">Université de Pittsburgh</orgName></affiliation></author><author><name sortKey="Lee, Yong J" sort="Lee, Yong J" uniqKey="Lee Y" first="Yong J" last="Lee">Yong J. Lee</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2003">2003</date><idno type="RBID">pubmed:12723971</idno><idno type="pmid">12723971</idno><idno type="doi">10.1042/BJ20030275</idno><idno type="pmc">PMC1223534</idno><idno type="wicri:Area/Main/Corpus">000F38</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000F38</idno><idno type="wicri:Area/Main/Curation">000F38</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000F38</idno><idno type="wicri:Area/Main/Exploration">000F38</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Differential role of glutaredoxin and thioredoxin in metabolic oxidative stress-induced activation of apoptosis signal-regulating kinase 1.</title><author><name sortKey="Song, Jae J" sort="Song, Jae J" uniqKey="Song J" first="Jae J" last="Song">Jae J. Song</name><affiliation wicri:level="4"><nlm:affiliation>Department of Surgery and Cancer Institute, Hillman Cancer Center, University of Pittsburgh, Pittsburgh, PA 15213, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Surgery and Cancer Institute, Hillman Cancer Center, University of Pittsburgh, Pittsburgh, PA 15213</wicri:regionArea><placeName><region type="state">Pennsylvanie</region><settlement type="city">Pittsburgh</settlement></placeName><orgName type="university">Université de Pittsburgh</orgName></affiliation></author><author><name sortKey="Lee, Yong J" sort="Lee, Yong J" uniqKey="Lee Y" first="Yong J" last="Lee">Yong J. Lee</name></author></analytic><series><title level="j">The Biochemical journal</title><idno type="ISSN">0264-6021</idno><imprint><date when="2003" type="published">2003</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenoviridae (genetics)</term><term>Buthionine Sulfoximine (pharmacology)</term><term>Catalase (metabolism)</term><term>Enzyme Activation (MeSH)</term><term>Genetic Vectors (MeSH)</term><term>Glucose (metabolism)</term><term>Glutaredoxins (MeSH)</term><term>Humans (MeSH)</term><term>MAP Kinase Kinase Kinase 5 (MeSH)</term><term>MAP Kinase Kinase Kinases (metabolism)</term><term>Male (MeSH)</term><term>Oxidative Stress (MeSH)</term><term>Oxidoreductases (MeSH)</term><term>Proteins (physiology)</term><term>Thioredoxins (metabolism)</term><term>Tumor Cells, Cultured (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Activation enzymatique (MeSH)</term><term>Adenoviridae (génétique)</term><term>Buthionine sulfoximine (pharmacologie)</term><term>Catalase (métabolisme)</term><term>Cellules cancéreuses en culture (MeSH)</term><term>Glucose (métabolisme)</term><term>Glutarédoxines (MeSH)</term><term>Humains (MeSH)</term><term>MAP Kinase Kinase Kinase 5 (MeSH)</term><term>MAP Kinase Kinase Kinases (métabolisme)</term><term>Mâle (MeSH)</term><term>Oxidoreductases (MeSH)</term><term>Protéines (physiologie)</term><term>Stress oxydatif (MeSH)</term><term>Thiorédoxines (métabolisme)</term><term>Vecteurs génétiques (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Catalase</term><term>Glucose</term><term>MAP Kinase Kinase Kinases</term><term>Thioredoxins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Buthionine Sulfoximine</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Adenoviridae</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Adenoviridae</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Catalase</term><term>Glucose</term><term>MAP Kinase Kinase Kinases</term><term>Thiorédoxines</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Buthionine sulfoximine</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Protéines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Proteins</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Enzyme Activation</term><term>Genetic Vectors</term><term>Glutaredoxins</term><term>Humans</term><term>MAP Kinase Kinase Kinase 5</term><term>Male</term><term>Oxidative Stress</term><term>Oxidoreductases</term><term>Tumor Cells, Cultured</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Activation enzymatique</term><term>Cellules cancéreuses en culture</term><term>Glutarédoxines</term><term>Humains</term><term>MAP Kinase Kinase Kinase 5</term><term>Mâle</term><term>Oxidoreductases</term><term>Stress oxydatif</term><term>Vecteurs génétiques</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Redox-sensing molecules such as thioredoxin (TRX) and glutaredoxin (GRX) bind to apoptosis signal-regulating kinase 1 (ASK1) and suppress its activation. Glucose deprivation disrupted the interaction between TRX/GRX and ASK1 and subsequently activated the ASK1-stress-activated protein kinase/extracellular-signal-regulated kinase kinase-c-Jun N-terminal kinase 1 (JNK1) signal-transduction pathway. L-Buthionine-( S, R )-sulphoximine, which decreases intracellular glutathione content, enhanced glucose deprivation-induced activation of JNK1 by promoting the dissociation of TRX, but not GRX, from ASK1. Treatment of cells with exogenous glutathione disulphide ester resulted in the dissociation of GRX, but not TRX, from ASK1 and the subsequent activation of JNK1. Nonetheless, overexpression of calatase, an H(2)O(2) scavenger, inhibited JNK1 activation and cytotoxicity as well as the dissociation of TRX and GRX from ASK1 during combined glucose deprivation and L-buthionine-( S, R )-sulphoximine treatment. Taken together, glucose deprivation-induced metabolic oxidative stress may activate ASK1 through two different pathways: glutathione-dependent GRX-ASK1 and glutathione-independent TRX-ASK1 pathways.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">12723971</PMID><DateCompleted><Year>2003</Year><Month>09</Month><Day>03</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0264-6021</ISSN><JournalIssue CitedMedium="Print"><Volume>373</Volume><Issue>Pt 3</Issue><PubDate><Year>2003</Year><Month>Aug</Month><Day>01</Day></PubDate></JournalIssue><Title>The Biochemical journal</Title><ISOAbbreviation>Biochem J</ISOAbbreviation></Journal><ArticleTitle>Differential role of glutaredoxin and thioredoxin in metabolic oxidative stress-induced activation of apoptosis signal-regulating kinase 1.</ArticleTitle><Pagination><MedlinePgn>845-53</MedlinePgn></Pagination><Abstract><AbstractText>Redox-sensing molecules such as thioredoxin (TRX) and glutaredoxin (GRX) bind to apoptosis signal-regulating kinase 1 (ASK1) and suppress its activation. Glucose deprivation disrupted the interaction between TRX/GRX and ASK1 and subsequently activated the ASK1-stress-activated protein kinase/extracellular-signal-regulated kinase kinase-c-Jun N-terminal kinase 1 (JNK1) signal-transduction pathway. L-Buthionine-( S, R )-sulphoximine, which decreases intracellular glutathione content, enhanced glucose deprivation-induced activation of JNK1 by promoting the dissociation of TRX, but not GRX, from ASK1. Treatment of cells with exogenous glutathione disulphide ester resulted in the dissociation of GRX, but not TRX, from ASK1 and the subsequent activation of JNK1. Nonetheless, overexpression of calatase, an H(2)O(2) scavenger, inhibited JNK1 activation and cytotoxicity as well as the dissociation of TRX and GRX from ASK1 during combined glucose deprivation and L-buthionine-( S, R )-sulphoximine treatment. Taken together, glucose deprivation-induced metabolic oxidative stress may activate ASK1 through two different pathways: glutathione-dependent GRX-ASK1 and glutathione-independent TRX-ASK1 pathways.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Song</LastName><ForeName>Jae J</ForeName><Initials>JJ</Initials><AffiliationInfo><Affiliation>Department of Surgery and Cancer Institute, Hillman Cancer Center, University of Pittsburgh, Pittsburgh, PA 15213, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Yong J</ForeName><Initials>YJ</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>CA48000</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>CA95191</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Biochem J</MedlineTA><NlmUniqueID>2984726R</NlmUniqueID><ISSNLinking>0264-6021</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C516005">GLRX protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011506">Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>5072-26-4</RegistryNumber><NameOfSubstance UI="D019328">Buthionine Sulfoximine</NameOfSubstance></Chemical><Chemical><RegistryNumber>52500-60-4</RegistryNumber><NameOfSubstance UI="D013879">Thioredoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.-</RegistryNumber><NameOfSubstance UI="D010088">Oxidoreductases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.11.1.6</RegistryNumber><NameOfSubstance UI="D002374">Catalase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.25</RegistryNumber><NameOfSubstance UI="D048848">MAP Kinase Kinase Kinase 5</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.25</RegistryNumber><NameOfSubstance UI="D020930">MAP Kinase Kinase Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.25</RegistryNumber><NameOfSubstance UI="C482858">MAP3K5 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>IY9XDZ35W2</RegistryNumber><NameOfSubstance UI="D005947">Glucose</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000256" MajorTopicYN="N">Adenoviridae</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019328" MajorTopicYN="N">Buthionine Sulfoximine</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002374" MajorTopicYN="N">Catalase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004789" MajorTopicYN="N">Enzyme Activation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005822" MajorTopicYN="N">Genetic Vectors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005947" MajorTopicYN="N">Glucose</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D048848" MajorTopicYN="N">MAP Kinase Kinase Kinase 5</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020930" MajorTopicYN="N">MAP Kinase Kinase Kinases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018384" MajorTopicYN="Y">Oxidative Stress</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010088" MajorTopicYN="Y">Oxidoreductases</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011506" MajorTopicYN="N">Proteins</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013879" MajorTopicYN="N">Thioredoxins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014407" MajorTopicYN="N">Tumor Cells, Cultured</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="accepted"><Year>2003</Year><Month>04</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2003</Year><Month>04</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="received"><Year>2003</Year><Month>02</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2003</Year><Month>5</Month><Day>2</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2003</Year><Month>9</Month><Day>4</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2003</Year><Month>5</Month><Day>2</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">12723971</ArticleId><ArticleId IdType="doi">10.1042/BJ20030275</ArticleId><ArticleId IdType="pii">BJ20030275</ArticleId><ArticleId IdType="pmc">PMC1223534</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Eur J Clin Invest. 1999 Mar;29(3):238-45</Citation><ArticleIdList><ArticleId IdType="pubmed">10202381</ArticleId></ArticleIdList></Reference><Reference><Citation>Free Radic Biol Med. 1998 Mar 1;24(4):556-62</Citation><ArticleIdList><ArticleId IdType="pubmed">9559867</ArticleId></ArticleIdList></Reference><Reference><Citation>Proc Natl Acad Sci U S A. 1999 Jul 20;96(15):8511-5</Citation><ArticleIdList><ArticleId IdType="pubmed">10411906</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Cell Biol. 2000 Mar;20(6):2198-208</Citation><ArticleIdList><ArticleId IdType="pubmed">10688666</ArticleId></ArticleIdList></Reference><Reference><Citation>Free Radic Biol Med. 2000 Feb 15;28(4):575-84</Citation><ArticleIdList><ArticleId IdType="pubmed">10719239</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 2000 Aug 25;275(34):26556-65</Citation><ArticleIdList><ArticleId IdType="pubmed">10854441</ArticleId></ArticleIdList></Reference><Reference><Citation>Free Radic Biol Med. 2000 Aug;29(3-4):323-33</Citation><ArticleIdList><ArticleId IdType="pubmed">11035261</ArticleId></ArticleIdList></Reference><Reference><Citation>EMBO J. 2000 Oct 2;19(19):5157-66</Citation><ArticleIdList><ArticleId IdType="pubmed">11013218</ArticleId></ArticleIdList></Reference><Reference><Citation>J Cell Sci. 2001 Feb;114(Pt 4):677-84</Citation><ArticleIdList><ArticleId IdType="pubmed">11171373</ArticleId></ArticleIdList></Reference><Reference><Citation>EMBO Rep. 2001 Mar;2(3):222-8</Citation><ArticleIdList><ArticleId IdType="pubmed">11266364</ArticleId></ArticleIdList></Reference><Reference><Citation>Oncogene. 2001 Apr 30;20(19):2336-46</Citation><ArticleIdList><ArticleId IdType="pubmed">11402331</ArticleId></ArticleIdList></Reference><Reference><Citation>EMBO J. 1998 May 1;17(9):2596-606</Citation><ArticleIdList><ArticleId IdType="pubmed">9564042</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 1998 Aug 28;273(35):22681-92</Citation><ArticleIdList><ArticleId IdType="pubmed">9712898</ArticleId></ArticleIdList></Reference><Reference><Citation>Science. 1998 Sep 18;281(5384):1860-3</Citation><ArticleIdList><ArticleId IdType="pubmed">9743501</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 1998 Nov 6;273(45):29857-63</Citation><ArticleIdList><ArticleId IdType="pubmed">9792702</ArticleId></ArticleIdList></Reference><Reference><Citation>Biochemistry. 1998 Dec 8;37(49):17145-56</Citation><ArticleIdList><ArticleId IdType="pubmed">9860827</ArticleId></ArticleIdList></Reference><Reference><Citation>Free Radic Biol Med. 1999 Feb;26(3-4):419-30</Citation><ArticleIdList><ArticleId IdType="pubmed">9895234</ArticleId></ArticleIdList></Reference><Reference><Citation>Proc Natl Acad Sci U S A. 1999 Feb 16;96(4):1252-6</Citation><ArticleIdList><ArticleId IdType="pubmed">9990010</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell Signal. 1999 Jan;11(1):1-14</Citation><ArticleIdList><ArticleId IdType="pubmed">10206339</ArticleId></ArticleIdList></Reference><Reference><Citation>J Neurochem. 2001 Jun;77(6):1496-507</Citation><ArticleIdList><ArticleId IdType="pubmed">11413233</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 2001 Oct 19;276(42):39103-6</Citation><ArticleIdList><ArticleId IdType="pubmed">11495919</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 2002 Nov 29;277(48):46566-75</Citation><ArticleIdList><ArticleId IdType="pubmed">12244106</ArticleId></ArticleIdList></Reference><Reference><Citation>Antisense Nucleic Acid Drug Dev. 2002 Oct;12(5):327-40</Citation><ArticleIdList><ArticleId IdType="pubmed">12477282</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 1982 Nov 25;257(22):13704-12</Citation><ArticleIdList><ArticleId IdType="pubmed">6128339</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 1989 Aug 25;264(24):13963-6</Citation><ArticleIdList><ArticleId IdType="pubmed">2668278</ArticleId></ArticleIdList></Reference><Reference><Citation>Biochem Biophys Res Commun. 1992 Aug 14;186(3):1220-6</Citation><ArticleIdList><ArticleId IdType="pubmed">1510657</ArticleId></ArticleIdList></Reference><Reference><Citation>Proc Natl Acad Sci U S A. 1993 Nov 1;90(21):9993-7</Citation><ArticleIdList><ArticleId IdType="pubmed">8234347</ArticleId></ArticleIdList></Reference><Reference><Citation>EMBO J. 1994 Jan 1;13(1):138-46</Citation><ArticleIdList><ArticleId IdType="pubmed">8306957</ArticleId></ArticleIdList></Reference><Reference><Citation>Eur J Biochem. 1995 Jan 15;227(1-2):27-34</Citation><ArticleIdList><ArticleId IdType="pubmed">7851394</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol. 1995 Apr 1;154(7):3194-203</Citation><ArticleIdList><ArticleId IdType="pubmed">7897207</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 1996 Mar 29;271(13):7269-72</Citation><ArticleIdList><ArticleId IdType="pubmed">8631739</ArticleId></ArticleIdList></Reference><Reference><Citation>Science. 1997 Jan 3;275(5296):90-4</Citation><ArticleIdList><ArticleId IdType="pubmed">8974401</ArticleId></ArticleIdList></Reference><Reference><Citation>J Virol. 1997 Mar;71(3):1842-9</Citation><ArticleIdList><ArticleId IdType="pubmed">9032314</ArticleId></ArticleIdList></Reference><Reference><Citation>Nucleic Acids Res. 1997 Apr 15;25(8):1469-75</Citation><ArticleIdList><ArticleId IdType="pubmed">9092651</ArticleId></ArticleIdList></Reference><Reference><Citation>Trends Biochem Sci. 1997 Jun;22(6):207-10</Citation><ArticleIdList><ArticleId IdType="pubmed">9204707</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell. 1997 Jun 27;89(7):1067-76</Citation><ArticleIdList><ArticleId IdType="pubmed">9215629</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Cell Biol. 1997 Aug;17(8):4792-800</Citation><ArticleIdList><ArticleId IdType="pubmed">9234735</ArticleId></ArticleIdList></Reference><Reference><Citation>Proc Natl Acad Sci U S A. 1997 Aug 5;94(16):8445-9</Citation><ArticleIdList><ArticleId IdType="pubmed">9237996</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 1998 Feb 27;273(9):5294-9</Citation><ArticleIdList><ArticleId IdType="pubmed">9478987</ArticleId></ArticleIdList></Reference><Reference><Citation>Science. 1998 Mar 13;279(5357):1718-21</Citation><ArticleIdList><ArticleId IdType="pubmed">9497290</ArticleId></ArticleIdList></Reference><Reference><Citation>Brain Res. 1999 Apr 24;826(1):53-62</Citation><ArticleIdList><ArticleId IdType="pubmed">10216196</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Pennsylvanie</li></region><settlement><li>Pittsburgh</li></settlement><orgName><li>Université de Pittsburgh</li></orgName></list><tree><noCountry><name sortKey="Lee, Yong J" sort="Lee, Yong J" uniqKey="Lee Y" first="Yong J" last="Lee">Yong J. Lee</name></noCountry><country name="États-Unis"><region name="Pennsylvanie"><name sortKey="Song, Jae J" sort="Song, Jae J" uniqKey="Song J" first="Jae J" last="Song">Jae J. Song</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Bois/explor/GlutaredoxinV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000F43 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000F43 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Bois
|area= GlutaredoxinV1
|flux= Main
|étape= Exploration
|type= RBID
|clé= pubmed:12723971
|texte= Differential role of glutaredoxin and thioredoxin in metabolic oxidative stress-induced activation of apoptosis signal-regulating kinase 1.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:12723971" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \
| NlmPubMed2Wicri -a GlutaredoxinV1
| This area was generated with Dilib version V0.6.37. |  |