GlutaredoxinV1, Main, Exploration, bibRecord, 000C53

Targeted disruption of the glutaredoxin 1 gene does not sensitize adult mice to tissue injury induced by ischemia/reperfusion and hyperoxia.

Identifieur interne : 000C53 ( Main/Exploration ); précédent : 000C52; suivant : 000C54

Targeted disruption of the glutaredoxin 1 gene does not sensitize adult mice to tissue injury induced by ischemia/reperfusion and hyperoxia.

Auteurs : Ye-Shih Ho [États-Unis] ; Ye Xiong ; Dorothy S. Ho ; Jinping Gao ; Balvin H L. Chua ; Harish Pai ; John J. Mieyal

Source :

Free radical biology & medicine [ 0891-5849 ] ; 2007.

RBID : pubmed:17893043

Descripteurs français

KwdFr :
- Animaux (MeSH), Apoptose (effets des médicaments et des substances chimiques), Apoptose (physiologie), Ciblage de gène (méthodes), Dactinomycine (pharmacologie), Diquat (toxicité), Disulfures (métabolisme), Espèces réactives de l'oxygène (composition chimique), Espèces réactives de l'oxygène (métabolisme), Facteur de nécrose tumorale alpha (pharmacologie), Fibroblastes (MeSH), Glutarédoxines (composition chimique), Glutarédoxines (déficit), Glutarédoxines (génétique), Glutarédoxines (métabolisme), Hyperoxie (anatomopathologie), Hyperoxie (enzymologie), Hyperoxie (génétique), Lignée cellulaire (MeSH), Lésion de reperfusion myocardique (anatomopathologie), Lésion de reperfusion myocardique (enzymologie), Lésion de reperfusion myocardique (génétique), Myocarde (anatomopathologie), Myocarde (enzymologie), Paraquat (toxicité), Peroxyde d'hydrogène (toxicité), Poumon (anatomopathologie), Poumon (métabolisme), Poumon (vascularisation), Souris (MeSH), Souris de lignée C57BL (MeSH), Souris knockout (MeSH), Stress oxydatif (MeSH), Tétraméthyl-diazènedicarboxamide (composition chimique).
MESH :
- anatomopathologie : Hyperoxie, Lésion de reperfusion myocardique, Myocarde, Poumon.
- composition chimique : Espèces réactives de l'oxygène, Glutarédoxines, Tétraméthyl-diazènedicarboxamide.
- déficit : Glutarédoxines.
- effets des médicaments et des substances chimiques : Apoptose.
- enzymologie : Hyperoxie, Lésion de reperfusion myocardique, Myocarde.
- génétique : Glutarédoxines, Hyperoxie, Lésion de reperfusion myocardique.
- métabolisme : Disulfures, Espèces réactives de l'oxygène, Glutarédoxines, Poumon.
- méthodes : Ciblage de gène.
- pharmacologie : Dactinomycine, Facteur de nécrose tumorale alpha.
- physiologie : Apoptose.
- toxicité : Diquat, Paraquat, Peroxyde d'hydrogène.
- vascularisation : Poumon.
- Animaux, Fibroblastes, Lignée cellulaire, Souris, Souris de lignée C57BL, Souris knockout, Stress oxydatif.

English descriptors

KwdEn :
- Animals (MeSH), Apoptosis (drug effects), Apoptosis (physiology), Cell Line (MeSH), Dactinomycin (pharmacology), Diamide (chemistry), Diquat (toxicity), Disulfides (metabolism), Fibroblasts (MeSH), Gene Targeting (methods), Glutaredoxins (chemistry), Glutaredoxins (deficiency), Glutaredoxins (genetics), Glutaredoxins (metabolism), Hydrogen Peroxide (toxicity), Hyperoxia (enzymology), Hyperoxia (genetics), Hyperoxia (pathology), Lung (blood supply), Lung (metabolism), Lung (pathology), Mice (MeSH), Mice, Inbred C57BL (MeSH), Mice, Knockout (MeSH), Myocardial Reperfusion Injury (enzymology), Myocardial Reperfusion Injury (genetics), Myocardial Reperfusion Injury (pathology), Myocardium (enzymology), Myocardium (pathology), Oxidative Stress (MeSH), Paraquat (toxicity), Reactive Oxygen Species (chemistry), Reactive Oxygen Species (metabolism), Tumor Necrosis Factor-alpha (pharmacology).
MESH :
- chemical , chemistry : Diamide, Glutaredoxins, Reactive Oxygen Species.
- chemical , deficiency : Glutaredoxins.
- chemical , genetics : Glutaredoxins.
- chemical , metabolism : Disulfides, Glutaredoxins, Reactive Oxygen Species.
- chemical , pharmacology : Dactinomycin, Tumor Necrosis Factor-alpha.
- blood supply : Lung.
- drug effects : Apoptosis.
- enzymology : Hyperoxia, Myocardial Reperfusion Injury, Myocardium.
- genetics : Hyperoxia, Myocardial Reperfusion Injury.
- metabolism : Lung.
- methods : Gene Targeting.
- pathology : Hyperoxia, Lung, Myocardial Reperfusion Injury, Myocardium.
- physiology : Apoptosis.
- chemical , toxicity : Diquat, Hydrogen Peroxide, Paraquat.
- Animals, Cell Line, Fibroblasts, Mice, Mice, Inbred C57BL, Mice, Knockout, Oxidative Stress.

Abstract

To understand the physiological function of glutaredoxin, a thiotransferase catalyzing the reduction of mixed disulfides of protein and glutathione, we generated a line of knockout mice deficient in the cytosolic glutaredoxin 1 (Grx1). To our surprise, mice deficient in Grx1 were not more susceptible to acute oxidative insults in models of heart and lung injury induced by ischemia/reperfusion and hyperoxia, respectively, suggesting that either changes in S-glutathionylation status of cytosolic proteins are not the major cause of such tissue injury or developmental adaptation in the Glrx1-knockout animals alters the response to oxidative insult. In contrast, mouse embryonic fibroblasts (MEFs) isolated from Grx1-deficient mice displayed an increased vulnerability to diquat and paraquat, but they were not more susceptible to cell death induced by hydrogen peroxide (H(2)O(2)) and diamide. A deficiency in Grx1 also sensitized MEFs to protein S-glutathionylation in response to H(2)O(2) treatment and retarded deglutathionylation of the S-glutathionylated proteins, especially for a single prominent protein band. Additional experiments showed that MEFs lacking Grx1 were more tolerant to apoptosis induced by tumor necrosis factor alphaplus actinomycin D. These findings suggest that various oxidants may damage the cells via distinct mechanisms in which the action of Grx1 may or may not be protective and Grx1 may exert its function on specific target proteins.

DOI: 10.1016/j.freeradbiomed.2007.07.025
PubMed: 17893043
PubMed Central: PMC2196211

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000C42
to stream Main, to step Curation: 000C42

Le document en format XML

<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Targeted disruption of the glutaredoxin 1 gene does not sensitize adult mice to tissue injury induced by ischemia/reperfusion and hyperoxia.</title>
<author><name sortKey="Ho, Ye Shih" sort="Ho, Ye Shih" uniqKey="Ho Y" first="Ye-Shih" last="Ho">Ye-Shih Ho</name>
<affiliation wicri:level="2"><nlm:affiliation>Institute of Environmental Health Sciences and Department of Biochemistry and Molecular Biology, Wayne State University, Detroit, MI 48201, USA. yho@wayne.edu</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Institute of Environmental Health Sciences and Department of Biochemistry and Molecular Biology, Wayne State University, Detroit, MI 48201</wicri:regionArea>
<placeName><region type="state">Michigan</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Xiong, Ye" sort="Xiong, Ye" uniqKey="Xiong Y" first="Ye" last="Xiong">Ye Xiong</name>
</author>
<author><name sortKey="Ho, Dorothy S" sort="Ho, Dorothy S" uniqKey="Ho D" first="Dorothy S" last="Ho">Dorothy S. Ho</name>
</author>
<author><name sortKey="Gao, Jinping" sort="Gao, Jinping" uniqKey="Gao J" first="Jinping" last="Gao">Jinping Gao</name>
</author>
<author><name sortKey="Chua, Balvin H L" sort="Chua, Balvin H L" uniqKey="Chua B" first="Balvin H L" last="Chua">Balvin H L. Chua</name>
</author>
<author><name sortKey="Pai, Harish" sort="Pai, Harish" uniqKey="Pai H" first="Harish" last="Pai">Harish Pai</name>
</author>
<author><name sortKey="Mieyal, John J" sort="Mieyal, John J" uniqKey="Mieyal J" first="John J" last="Mieyal">John J. Mieyal</name>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PubMed</idno>
<date when="2007">2007</date>
<idno type="RBID">pubmed:17893043</idno>
<idno type="pmid">17893043</idno>
<idno type="doi">10.1016/j.freeradbiomed.2007.07.025</idno>
<idno type="pmc">PMC2196211</idno>
<idno type="wicri:Area/Main/Corpus">000C42</idno>
<idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000C42</idno>
<idno type="wicri:Area/Main/Curation">000C42</idno>
<idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000C42</idno>
<idno type="wicri:Area/Main/Exploration">000C42</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en">Targeted disruption of the glutaredoxin 1 gene does not sensitize adult mice to tissue injury induced by ischemia/reperfusion and hyperoxia.</title>
<author><name sortKey="Ho, Ye Shih" sort="Ho, Ye Shih" uniqKey="Ho Y" first="Ye-Shih" last="Ho">Ye-Shih Ho</name>
<affiliation wicri:level="2"><nlm:affiliation>Institute of Environmental Health Sciences and Department of Biochemistry and Molecular Biology, Wayne State University, Detroit, MI 48201, USA. yho@wayne.edu</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Institute of Environmental Health Sciences and Department of Biochemistry and Molecular Biology, Wayne State University, Detroit, MI 48201</wicri:regionArea>
<placeName><region type="state">Michigan</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Xiong, Ye" sort="Xiong, Ye" uniqKey="Xiong Y" first="Ye" last="Xiong">Ye Xiong</name>
</author>
<author><name sortKey="Ho, Dorothy S" sort="Ho, Dorothy S" uniqKey="Ho D" first="Dorothy S" last="Ho">Dorothy S. Ho</name>
</author>
<author><name sortKey="Gao, Jinping" sort="Gao, Jinping" uniqKey="Gao J" first="Jinping" last="Gao">Jinping Gao</name>
</author>
<author><name sortKey="Chua, Balvin H L" sort="Chua, Balvin H L" uniqKey="Chua B" first="Balvin H L" last="Chua">Balvin H L. Chua</name>
</author>
<author><name sortKey="Pai, Harish" sort="Pai, Harish" uniqKey="Pai H" first="Harish" last="Pai">Harish Pai</name>
</author>
<author><name sortKey="Mieyal, John J" sort="Mieyal, John J" uniqKey="Mieyal J" first="John J" last="Mieyal">John J. Mieyal</name>
</author>
</analytic>
<series><title level="j">Free radical biology & medicine</title>
<idno type="ISSN">0891-5849</idno>
<imprint><date when="2007" type="published">2007</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>Apoptosis (drug effects)</term>
<term>Apoptosis (physiology)</term>
<term>Cell Line (MeSH)</term>
<term>Dactinomycin (pharmacology)</term>
<term>Diamide (chemistry)</term>
<term>Diquat (toxicity)</term>
<term>Disulfides (metabolism)</term>
<term>Fibroblasts (MeSH)</term>
<term>Gene Targeting (methods)</term>
<term>Glutaredoxins (chemistry)</term>
<term>Glutaredoxins (deficiency)</term>
<term>Glutaredoxins (genetics)</term>
<term>Glutaredoxins (metabolism)</term>
<term>Hydrogen Peroxide (toxicity)</term>
<term>Hyperoxia (enzymology)</term>
<term>Hyperoxia (genetics)</term>
<term>Hyperoxia (pathology)</term>
<term>Lung (blood supply)</term>
<term>Lung (metabolism)</term>
<term>Lung (pathology)</term>
<term>Mice (MeSH)</term>
<term>Mice, Inbred C57BL (MeSH)</term>
<term>Mice, Knockout (MeSH)</term>
<term>Myocardial Reperfusion Injury (enzymology)</term>
<term>Myocardial Reperfusion Injury (genetics)</term>
<term>Myocardial Reperfusion Injury (pathology)</term>
<term>Myocardium (enzymology)</term>
<term>Myocardium (pathology)</term>
<term>Oxidative Stress (MeSH)</term>
<term>Paraquat (toxicity)</term>
<term>Reactive Oxygen Species (chemistry)</term>
<term>Reactive Oxygen Species (metabolism)</term>
<term>Tumor Necrosis Factor-alpha (pharmacology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Apoptose (effets des médicaments et des substances chimiques)</term>
<term>Apoptose (physiologie)</term>
<term>Ciblage de gène (méthodes)</term>
<term>Dactinomycine (pharmacologie)</term>
<term>Diquat (toxicité)</term>
<term>Disulfures (métabolisme)</term>
<term>Espèces réactives de l'oxygène (composition chimique)</term>
<term>Espèces réactives de l'oxygène (métabolisme)</term>
<term>Facteur de nécrose tumorale alpha (pharmacologie)</term>
<term>Fibroblastes (MeSH)</term>
<term>Glutarédoxines (composition chimique)</term>
<term>Glutarédoxines (déficit)</term>
<term>Glutarédoxines (génétique)</term>
<term>Glutarédoxines (métabolisme)</term>
<term>Hyperoxie (anatomopathologie)</term>
<term>Hyperoxie (enzymologie)</term>
<term>Hyperoxie (génétique)</term>
<term>Lignée cellulaire (MeSH)</term>
<term>Lésion de reperfusion myocardique (anatomopathologie)</term>
<term>Lésion de reperfusion myocardique (enzymologie)</term>
<term>Lésion de reperfusion myocardique (génétique)</term>
<term>Myocarde (anatomopathologie)</term>
<term>Myocarde (enzymologie)</term>
<term>Paraquat (toxicité)</term>
<term>Peroxyde d'hydrogène (toxicité)</term>
<term>Poumon (anatomopathologie)</term>
<term>Poumon (métabolisme)</term>
<term>Poumon (vascularisation)</term>
<term>Souris (MeSH)</term>
<term>Souris de lignée C57BL (MeSH)</term>
<term>Souris knockout (MeSH)</term>
<term>Stress oxydatif (MeSH)</term>
<term>Tétraméthyl-diazènedicarboxamide (composition chimique)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Diamide</term>
<term>Glutaredoxins</term>
<term>Reactive Oxygen Species</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Glutaredoxins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Glutaredoxins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Disulfides</term>
<term>Glutaredoxins</term>
<term>Reactive Oxygen Species</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Dactinomycin</term>
<term>Tumor Necrosis Factor-alpha</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Hyperoxie</term>
<term>Lésion de reperfusion myocardique</term>
<term>Myocarde</term>
<term>Poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="blood supply" xml:lang="en"><term>Lung</term>
</keywords>
<keywords scheme="MESH" qualifier="composition chimique" xml:lang="fr"><term>Espèces réactives de l'oxygène</term>
<term>Glutarédoxines</term>
<term>Tétraméthyl-diazènedicarboxamide</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term>
</keywords>
<keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Glutarédoxines</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Apoptose</term>
</keywords>
<keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Hyperoxie</term>
<term>Lésion de reperfusion myocardique</term>
<term>Myocarde</term>
</keywords>
<keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Hyperoxia</term>
<term>Myocardial Reperfusion Injury</term>
<term>Myocardium</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Hyperoxia</term>
<term>Myocardial Reperfusion Injury</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Glutarédoxines</term>
<term>Hyperoxie</term>
<term>Lésion de reperfusion myocardique</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Lung</term>
</keywords>
<keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Gene Targeting</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Disulfures</term>
<term>Espèces réactives de l'oxygène</term>
<term>Glutarédoxines</term>
<term>Poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="méthodes" xml:lang="fr"><term>Ciblage de gène</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Hyperoxia</term>
<term>Lung</term>
<term>Myocardial Reperfusion Injury</term>
<term>Myocardium</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Dactinomycine</term>
<term>Facteur de nécrose tumorale alpha</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Apoptose</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Apoptosis</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Diquat</term>
<term>Hydrogen Peroxide</term>
<term>Paraquat</term>
</keywords>
<keywords scheme="MESH" qualifier="toxicité" xml:lang="fr"><term>Diquat</term>
<term>Paraquat</term>
<term>Peroxyde d'hydrogène</term>
</keywords>
<keywords scheme="MESH" qualifier="vascularisation" xml:lang="fr"><term>Poumon</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cell Line</term>
<term>Fibroblasts</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Knockout</term>
<term>Oxidative Stress</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Fibroblastes</term>
<term>Lignée cellulaire</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Souris knockout</term>
<term>Stress oxydatif</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">To understand the physiological function of glutaredoxin, a thiotransferase catalyzing the reduction of mixed disulfides of protein and glutathione, we generated a line of knockout mice deficient in the cytosolic glutaredoxin 1 (Grx1). To our surprise, mice deficient in Grx1 were not more susceptible to acute oxidative insults in models of heart and lung injury induced by ischemia/reperfusion and hyperoxia, respectively, suggesting that either changes in S-glutathionylation status of cytosolic proteins are not the major cause of such tissue injury or developmental adaptation in the Glrx1-knockout animals alters the response to oxidative insult. In contrast, mouse embryonic fibroblasts (MEFs) isolated from Grx1-deficient mice displayed an increased vulnerability to diquat and paraquat, but they were not more susceptible to cell death induced by hydrogen peroxide (H(2)O(2)) and diamide. A deficiency in Grx1 also sensitized MEFs to protein S-glutathionylation in response to H(2)O(2) treatment and retarded deglutathionylation of the S-glutathionylated proteins, especially for a single prominent protein band. Additional experiments showed that MEFs lacking Grx1 were more tolerant to apoptosis induced by tumor necrosis factor alphaplus actinomycin D. These findings suggest that various oxidants may damage the cells via distinct mechanisms in which the action of Grx1 may or may not be protective and Grx1 may exert its function on specific target proteins.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17893043</PMID>
<DateCompleted><Year>2008</Year>
<Month>02</Month>
<Day>19</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0891-5849</ISSN>
<JournalIssue CitedMedium="Print"><Volume>43</Volume>
<Issue>9</Issue>
<PubDate><Year>2007</Year>
<Month>Nov</Month>
<Day>01</Day>
</PubDate>
</JournalIssue>
<Title>Free radical biology & medicine</Title>
<ISOAbbreviation>Free Radic Biol Med</ISOAbbreviation>
</Journal>
<ArticleTitle>Targeted disruption of the glutaredoxin 1 gene does not sensitize adult mice to tissue injury induced by ischemia/reperfusion and hyperoxia.</ArticleTitle>
<Pagination><MedlinePgn>1299-312</MedlinePgn>
</Pagination>
<Abstract><AbstractText>To understand the physiological function of glutaredoxin, a thiotransferase catalyzing the reduction of mixed disulfides of protein and glutathione, we generated a line of knockout mice deficient in the cytosolic glutaredoxin 1 (Grx1). To our surprise, mice deficient in Grx1 were not more susceptible to acute oxidative insults in models of heart and lung injury induced by ischemia/reperfusion and hyperoxia, respectively, suggesting that either changes in S-glutathionylation status of cytosolic proteins are not the major cause of such tissue injury or developmental adaptation in the Glrx1-knockout animals alters the response to oxidative insult. In contrast, mouse embryonic fibroblasts (MEFs) isolated from Grx1-deficient mice displayed an increased vulnerability to diquat and paraquat, but they were not more susceptible to cell death induced by hydrogen peroxide (H(2)O(2)) and diamide. A deficiency in Grx1 also sensitized MEFs to protein S-glutathionylation in response to H(2)O(2) treatment and retarded deglutathionylation of the S-glutathionylated proteins, especially for a single prominent protein band. Additional experiments showed that MEFs lacking Grx1 were more tolerant to apoptosis induced by tumor necrosis factor alphaplus actinomycin D. These findings suggest that various oxidants may damage the cells via distinct mechanisms in which the action of Grx1 may or may not be protective and Grx1 may exert its function on specific target proteins.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ho</LastName>
<ForeName>Ye-Shih</ForeName>
<Initials>YS</Initials>
<AffiliationInfo><Affiliation>Institute of Environmental Health Sciences and Department of Biochemistry and Molecular Biology, Wayne State University, Detroit, MI 48201, USA. yho@wayne.edu</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Xiong</LastName>
<ForeName>Ye</ForeName>
<Initials>Y</Initials>
</Author>
<Author ValidYN="Y"><LastName>Ho</LastName>
<ForeName>Dorothy S</ForeName>
<Initials>DS</Initials>
</Author>
<Author ValidYN="Y"><LastName>Gao</LastName>
<ForeName>Jinping</ForeName>
<Initials>J</Initials>
</Author>
<Author ValidYN="Y"><LastName>Chua</LastName>
<ForeName>Balvin H L</ForeName>
<Initials>BH</Initials>
</Author>
<Author ValidYN="Y"><LastName>Pai</LastName>
<ForeName>Harish</ForeName>
<Initials>H</Initials>
</Author>
<Author ValidYN="Y"><LastName>Mieyal</LastName>
<ForeName>John J</ForeName>
<Initials>JJ</Initials>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>P30 ES006639-13</GrantID>
<Acronym>ES</Acronym>
<Agency>NIEHS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>AG024413</GrantID>
<Acronym>AG</Acronym>
<Agency>NIA NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>P01 AG015885</GrantID>
<Acronym>AG</Acronym>
<Agency>NIA NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>HL87271</GrantID>
<Acronym>HL</Acronym>
<Agency>NHLBI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R15 HL087271-01</GrantID>
<Acronym>HL</Acronym>
<Agency>NHLBI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R15 HL087271</GrantID>
<Acronym>HL</Acronym>
<Agency>NHLBI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>HL63317</GrantID>
<Acronym>HL</Acronym>
<Agency>NHLBI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>P30 ES06639</GrantID>
<Acronym>ES</Acronym>
<Agency>NIEHS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 HL063317-01</GrantID>
<Acronym>HL</Acronym>
<Agency>NHLBI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>P30 ES006639</GrantID>
<Acronym>ES</Acronym>
<Agency>NIEHS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 AG024413-03</GrantID>
<Acronym>AG</Acronym>
<Agency>NIA NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>AG15885</GrantID>
<Acronym>AG</Acronym>
<Agency>NIA NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>P01 AG015885-06</GrantID>
<Acronym>AG</Acronym>
<Agency>NIA NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 AG024413</GrantID>
<Acronym>AG</Acronym>
<Agency>NIA NIH HHS</Agency>
<Country>United States</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D052061">Research Support, N.I.H., Extramural</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>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2007</Year>
<Month>08</Month>
<Day>06</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Free Radic Biol Med</MedlineTA>
<NlmUniqueID>8709159</NlmUniqueID>
<ISSNLinking>0891-5849</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D004220">Disulfides</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C516006">Glrx protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D017382">Reactive Oxygen Species</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D014409">Tumor Necrosis Factor-alpha</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>10465-78-8</RegistryNumber>
<NameOfSubstance UI="D003958">Diamide</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>1CC1JFE158</RegistryNumber>
<NameOfSubstance UI="D003609">Dactinomycin</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>A9A615U4MP</RegistryNumber>
<NameOfSubstance UI="D004178">Diquat</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>BBX060AN9V</RegistryNumber>
<NameOfSubstance UI="D006861">Hydrogen Peroxide</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>PLG39H7695</RegistryNumber>
<NameOfSubstance UI="D010269">Paraquat</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D003609" MajorTopicYN="N">Dactinomycin</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D003958" MajorTopicYN="N">Diamide</DescriptorName>
<QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004178" MajorTopicYN="N">Diquat</DescriptorName>
<QualifierName UI="Q000633" MajorTopicYN="N">toxicity</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004220" MajorTopicYN="N">Disulfides</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005347" MajorTopicYN="N">Fibroblasts</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018390" MajorTopicYN="N">Gene Targeting</DescriptorName>
<QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName>
<QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName>
<QualifierName UI="Q000172" MajorTopicYN="Y">deficiency</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006861" MajorTopicYN="N">Hydrogen Peroxide</DescriptorName>
<QualifierName UI="Q000633" MajorTopicYN="N">toxicity</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018496" MajorTopicYN="N">Hyperoxia</DescriptorName>
<QualifierName UI="Q000201" MajorTopicYN="Y">enzymology</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008168" MajorTopicYN="N">Lung</DescriptorName>
<QualifierName UI="Q000098" MajorTopicYN="N">blood supply</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015428" MajorTopicYN="N">Myocardial Reperfusion Injury</DescriptorName>
<QualifierName UI="Q000201" MajorTopicYN="Y">enzymology</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009206" MajorTopicYN="N">Myocardium</DescriptorName>
<QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010269" MajorTopicYN="N">Paraquat</DescriptorName>
<QualifierName UI="Q000633" MajorTopicYN="N">toxicity</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName>
<QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014409" MajorTopicYN="N">Tumor Necrosis Factor-alpha</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
</MeshHeadingList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2007</Year>
<Month>05</Month>
<Day>03</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2007</Year>
<Month>06</Month>
<Day>22</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2007</Year>
<Month>07</Month>
<Day>21</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2007</Year>
<Month>9</Month>
<Day>26</Day>
<Hour>9</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2008</Year>
<Month>2</Month>
<Day>20</Day>
<Hour>9</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2007</Year>
<Month>9</Month>
<Day>26</Day>
<Hour>9</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">17893043</ArticleId>
<ArticleId IdType="pii">S0891-5849(07)00504-7</ArticleId>
<ArticleId IdType="doi">10.1016/j.freeradbiomed.2007.07.025</ArticleId>
<ArticleId IdType="pmc">PMC2196211</ArticleId>
<ArticleId IdType="mid">NIHMS31866</ArticleId>
</ArticleIdList>
<ReferenceList><Reference><Citation>J Biol Chem. 1997 Jan 31;272(5):2936-41</Citation>
<ArticleIdList><ArticleId IdType="pubmed">9006939</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Dev Biol. 1996 Aug 25;178(1):179-85</Citation>
<ArticleIdList><ArticleId IdType="pubmed">8812119</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Biochemistry. 1997 Mar 18;36(11):3199-206</Citation>
<ArticleIdList><ArticleId IdType="pubmed">9115997</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biol Chem. 1997 Oct 10;272(41):25935-40</Citation>
<ArticleIdList><ArticleId IdType="pubmed">9325327</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Gene. 1997 Sep 15;197(1-2):189-93</Citation>
<ArticleIdList><ArticleId IdType="pubmed">9332366</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>EMBO Rep. 2001 Aug;2(8):715-20</Citation>
<ArticleIdList><ArticleId IdType="pubmed">11493598</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Biochemistry. 2001 Nov 27;40(47):14134-42</Citation>
<ArticleIdList><ArticleId IdType="pubmed">11714266</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biol Chem. 2001 Dec 21;276(51):47763-6</Citation>
<ArticleIdList><ArticleId IdType="pubmed">11684673</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Arch Biochem Biophys. 2002 Sep 1;405(1):1-12</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12176051</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>Mol Cell Biol. 2003 Feb;23(3):916-22</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12529397</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2003 Apr 29;100(9):5103-6</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12697895</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Biochem J. 2003 Aug 1;373(Pt 3):845-53</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12723971</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Circulation. 1997 Nov 4;96(9 Suppl):II-216-20</Citation>
<ArticleIdList><ArticleId IdType="pubmed">9386101</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biol Chem. 1998 Jan 2;273(1):392-7</Citation>
<ArticleIdList><ArticleId IdType="pubmed">9417094</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 1998 Apr 14;95(8):4556-60</Citation>
<ArticleIdList><ArticleId IdType="pubmed">9539776</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biol Chem. 1998 Jun 19;273(25):15366-72</Citation>
<ArticleIdList><ArticleId IdType="pubmed">9624118</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Biochemistry. 1998 Dec 8;37(49):17145-56</Citation>
<ArticleIdList><ArticleId IdType="pubmed">9860827</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Science. 2006 Jun 30;312(5782):1882-3</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16809515</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2006 Aug 29;103(35):13086-91</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16916935</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Antioxid Redox Signal. 2007 Jan;9(1):25-47</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17115886</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Circ Res. 2007 Feb 2;100(2):213-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17185628</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biol Chem. 1999 Dec 3;274(49):34543-6</Citation>
<ArticleIdList><ArticleId IdType="pubmed">10574916</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Circ Res. 2000 Feb 18;86(3):264-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">10679476</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>FEBS Lett. 2000 Jun 30;476(1-2):52-4</Citation>
<ArticleIdList><ArticleId IdType="pubmed">10878249</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>Biochemistry. 2000 Aug 22;39(33):10319-29</Citation>
<ArticleIdList><ArticleId IdType="pubmed">10956021</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Free Radic Biol Med. 2000 Oct 1;29(7):589-96</Citation>
<ArticleIdList><ArticleId IdType="pubmed">11033410</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biol Chem. 2001 Jan 12;276(2):1335-44</Citation>
<ArticleIdList><ArticleId IdType="pubmed">11035035</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biol Chem. 2001 Jun 15;276(24):21618-26</Citation>
<ArticleIdList><ArticleId IdType="pubmed">11290748</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biol Chem. 2001 Jul 13;276(28):26269-75</Citation>
<ArticleIdList><ArticleId IdType="pubmed">11297543</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biol Chem. 2001 Aug 10;276(32):30374-80</Citation>
<ArticleIdList><ArticleId IdType="pubmed">11397793</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nature. 2003 Oct 30;425(6961):980-4</Citation>
<ArticleIdList><ArticleId IdType="pubmed">14586471</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biol Chem. 2003 Dec 12;278(50):50226-33</Citation>
<ArticleIdList><ArticleId IdType="pubmed">14522978</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Cell Biol. 2004 Feb 2;164(3):341-6</Citation>
<ArticleIdList><ArticleId IdType="pubmed">14757749</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Science. 2004 Apr 23;304(5670):596-600</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15105503</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biol Chem. 2004 Jul 9;279(28):29857-62</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15123696</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Biochemistry. 1979 Nov 27;18(24):5294-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">518835</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Am Rev Respir Dis. 1980 Jul;122(1):123-43</Citation>
<ArticleIdList><ArticleId IdType="pubmed">7406333</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 1980 Sep;77(9):5201-5</Citation>
<ArticleIdList><ArticleId IdType="pubmed">6159641</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Lab Invest. 1982 Nov;47(5):412-26</Citation>
<ArticleIdList><ArticleId IdType="pubmed">6290784</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Annu Rev Biochem. 1983;52:711-60</Citation>
<ArticleIdList><ArticleId IdType="pubmed">6137189</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Ann Intern Med. 1987 Oct;107(4):526-45</Citation>
<ArticleIdList><ArticleId IdType="pubmed">3307585</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biol Chem. 1988 Oct 25;263(30):15506-12</Citation>
<ArticleIdList><ArticleId IdType="pubmed">3170595</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>Cell. 1991 Jun 28;65(7):1153-63</Citation>
<ArticleIdList><ArticleId IdType="pubmed">2065352</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biol Chem. 1992 Nov 25;267(33):23937-41</Citation>
<ArticleIdList><ArticleId IdType="pubmed">1385428</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Adv Enzymol Relat Areas Mol Biol. 1993;66:149-201</Citation>
<ArticleIdList><ArticleId IdType="pubmed">8430514</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Biochemistry. 1993 Apr 6;32(13):3368-76</Citation>
<ArticleIdList><ArticleId IdType="pubmed">8461300</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Arch Biochem Biophys. 1993 Jun;303(2):474-82</Citation>
<ArticleIdList><ArticleId IdType="pubmed">8390225</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Annu Rev Biochem. 1993;62:797-821</Citation>
<ArticleIdList><ArticleId IdType="pubmed">8352601</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 1993 Sep 15;90(18):8424-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">8378314</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Curr Genet. 1994 Jul;26(1):15-20</Citation>
<ArticleIdList><ArticleId IdType="pubmed">7954891</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biochem. 1994 Jul;116(1):42-6</Citation>
<ArticleIdList><ArticleId IdType="pubmed">7798184</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 1995 Jul 3;92(14):6264-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">7603981</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Mol Cell Cardiol. 1998 Nov;30(11):2281-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">9925365</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Clin Invest. 1999 Apr;103(7):1055-66</Citation>
<ArticleIdList><ArticleId IdType="pubmed">10194479</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Free Radic Biol Med. 1999 Mar;26(5-6):770-6</Citation>
<ArticleIdList><ArticleId IdType="pubmed">10218667</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Biochemistry. 1999 May 18;38(20):6699-705</Citation>
<ArticleIdList><ArticleId IdType="pubmed">10350489</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Free Radic Biol Med. 2004 Dec 1;37(11):1736-43</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15528033</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biol Chem. 2004 Dec 3;279(49):50994-1001</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15448164</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Histol Histopathol. 2005 Jan;20(1):205-19</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15578439</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biol Chem. 2005 Feb 4;280(5):3125-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15590625</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Antioxid Redox Signal. 2005 Mar-Apr;7(3-4):348-66</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15706083</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Free Radic Biol Med. 2005 Jun 15;38(12):1543-52</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15917183</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Am J Respir Cell Mol Biol. 2006 Apr;34(4):481-6</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16399955</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Arch Biochem Biophys. 1996 Aug 15;332(2):288-94</Citation>
<ArticleIdList><ArticleId IdType="pubmed">8806737</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Mol Cell Cardiol. 1996 Aug;28(8):1759-67</Citation>
<ArticleIdList><ArticleId IdType="pubmed">8877785</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Arch Biochem Biophys. 1996 Nov 1;335(1):61-72</Citation>
<ArticleIdList><ArticleId IdType="pubmed">8914835</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
</PubmedData>
</pubmed>
<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Michigan</li>
</region>
</list>
<tree><noCountry><name sortKey="Chua, Balvin H L" sort="Chua, Balvin H L" uniqKey="Chua B" first="Balvin H L" last="Chua">Balvin H L. Chua</name>
<name sortKey="Gao, Jinping" sort="Gao, Jinping" uniqKey="Gao J" first="Jinping" last="Gao">Jinping Gao</name>
<name sortKey="Ho, Dorothy S" sort="Ho, Dorothy S" uniqKey="Ho D" first="Dorothy S" last="Ho">Dorothy S. Ho</name>
<name sortKey="Mieyal, John J" sort="Mieyal, John J" uniqKey="Mieyal J" first="John J" last="Mieyal">John J. Mieyal</name>
<name sortKey="Pai, Harish" sort="Pai, Harish" uniqKey="Pai H" first="Harish" last="Pai">Harish Pai</name>
<name sortKey="Xiong, Ye" sort="Xiong, Ye" uniqKey="Xiong Y" first="Ye" last="Xiong">Ye Xiong</name>
</noCountry>
<country name="États-Unis"><region name="Michigan"><name sortKey="Ho, Ye Shih" sort="Ho, Ye Shih" uniqKey="Ho Y" first="Ye-Shih" last="Ho">Ye-Shih Ho</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 000C53 | SxmlIndent | more

HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000C53 | 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:17893043
   |texte=   Targeted disruption of the glutaredoxin 1 gene does not sensitize adult mice to tissue injury induced by ischemia/reperfusion and hyperoxia.
}}

Pour générer des pages wiki

HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i   -Sk "pubmed:17893043" \
       | HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd   \
       | NlmPubMed2Wicri -a GlutaredoxinV1

This area was generated with Dilib version V0.6.37.
Data generation: Wed Nov 18 15:13:42 2020. Site generation: Wed Nov 18 15:16:12 2020

	Serveur d'exploration sur la glutarédoxine
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Serveur d'exploration sur la glutarédoxine

Targeted disruption of the glutaredoxin 1 gene does not sensitize adult mice to tissue injury induced by ischemia/reperfusion and hyperoxia.

Targeted disruption of the glutaredoxin 1 gene does not sensitize adult mice to tissue injury induced by ischemia/reperfusion and hyperoxia.

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki