PEP-1-glutaredoxin-1 induces dedifferentiation of rabbit articular chondrocytes by the endoplasmic reticulum stress-dependent ERK-1/2 pathway and the endoplasmic reticulum stress-independent p38 kinase and PI-3 kinase pathways.
Identifieur interne : 000239 ( Main/Exploration ); précédent : 000238; suivant : 000240PEP-1-glutaredoxin-1 induces dedifferentiation of rabbit articular chondrocytes by the endoplasmic reticulum stress-dependent ERK-1/2 pathway and the endoplasmic reticulum stress-independent p38 kinase and PI-3 kinase pathways.
Auteurs : Seon-Mi Yu [Corée du Sud] ; Yeon Joo Choi [Corée du Sud] ; Song Ja Kim [Corée du Sud]Source :
- International journal of biological macromolecules [ 1879-0003 ] ; 2018.
Descripteurs français
- KwdFr :
- 4H-1-Benzopyran-4-ones (pharmacologie), Animaux (MeSH), Cartilage articulaire (cytologie), Cartilage articulaire (effets des médicaments et des substances chimiques), Chondrocytes (cytologie), Chondrocytes (effets des médicaments et des substances chimiques), Différenciation cellulaire (effets des médicaments et des substances chimiques), Dédifférenciation cellulaire (effets des médicaments et des substances chimiques), Glutarédoxines (composition chimique), Glutarédoxines (génétique), Imidazoles (pharmacologie), Lapins (MeSH), Mercaptamine (analogues et dérivés), Mercaptamine (composition chimique), Morpholines (pharmacologie), Peptides (composition chimique), Peptides (génétique), Phosphatidylinositol 3-kinases (composition chimique), Phosphatidylinositol 3-kinases (génétique), Pyridines (pharmacologie), Stress du réticulum endoplasmique (effets des médicaments et des substances chimiques), Système de signalisation des MAP kinases (effets des médicaments et des substances chimiques).
- MESH :
- analogues et dérivés : Mercaptamine.
- composition chimique : Glutarédoxines, Mercaptamine, Peptides, Phosphatidylinositol 3-kinases.
- cytologie : Cartilage articulaire, Chondrocytes.
- effets des médicaments et des substances chimiques : Cartilage articulaire, Chondrocytes, Différenciation cellulaire, Dédifférenciation cellulaire, Stress du réticulum endoplasmique, Système de signalisation des MAP kinases.
- génétique : Glutarédoxines, Peptides, Phosphatidylinositol 3-kinases.
- pharmacologie : 4H-1-Benzopyran-4-ones, Imidazoles, Morpholines, Pyridines.
- Animaux, Lapins.
English descriptors
- KwdEn :
- Animals (MeSH), Cartilage, Articular (cytology), Cartilage, Articular (drug effects), Cell Dedifferentiation (drug effects), Cell Differentiation (drug effects), Chondrocytes (cytology), Chondrocytes (drug effects), Chromones (pharmacology), Cysteamine (analogs & derivatives), Cysteamine (chemistry), Endoplasmic Reticulum Stress (drug effects), Glutaredoxins (chemistry), Glutaredoxins (genetics), Imidazoles (pharmacology), MAP Kinase Signaling System (drug effects), Morpholines (pharmacology), Peptides (chemistry), Peptides (genetics), Phosphatidylinositol 3-Kinases (chemistry), Phosphatidylinositol 3-Kinases (genetics), Pyridines (pharmacology), Rabbits (MeSH).
- MESH :
- chemical , analogs & derivatives : Cysteamine.
- chemical , chemistry : Cysteamine, Glutaredoxins, Peptides, Phosphatidylinositol 3-Kinases.
- chemical , genetics : Glutaredoxins, Peptides, Phosphatidylinositol 3-Kinases.
- chemical , pharmacology : Chromones, Imidazoles, Morpholines, Pyridines.
- cytology : Cartilage, Articular, Chondrocytes.
- drug effects : Cartilage, Articular, Cell Dedifferentiation, Cell Differentiation, Chondrocytes, Endoplasmic Reticulum Stress, MAP Kinase Signaling System.
- Animals, Rabbits.
Abstract
Glutaredoxin-1 (GRX-1), belonging to the oxidoreductase family, is a component of the endogenous antioxidant defense system. In this study, we evaluated the effects of PEP-1-GRX-1 in rabbit articular chondrocytes. We found that PEP-1-GRX-1 causes a loss of the differentiated chondrocyte phenotype. PEP-1-GRX-1-treated cells exhibited decreases in type II collagen expression and sulfated-proteoglycan synthesis in a dose- and time-dependent manner. PEP-1-GRX-1 causes endoplasmic reticulum (ER)-stress, as evidenced by increases in ER stress marker proteins, i.e., glucose-regulated protein (GRP) 78, GRP 94, and phospho-eukaryotic initiation factor 2 (eIF2) α. These effects were inhibited by ER stress inhibitors. PEP-1-GRX-1 increased the phosphorylation of Akt, extracellular signal-regulated kinase (ERK)-1/2, and p38. Inhibition of ERK-1/2 by PD98059 prevented PEP-1-GRX-1-induced dedifferentiation and inhibited ER stress. The blockage of PI-3K/Akt or p38 kinase with SB203580 and LY294002 accelerated PEP-1-GRX-1-induced dedifferentiation, but did not have any effect on PEP-GRX-1-induced ER stress. Our results indicate that the ERK-1/2 pathway mediates chondrocyte dedifferentiation by PEP-GRX-1-induced ER stress. The PI-3K and p38 kinase pathways regulate PEP-1-GRX-1-induced chondrocyte dedifferentiation by an ER stress-independent pathway.
DOI: 10.1016/j.ijbiomac.2018.01.127
PubMed: 29366902
Affiliations:
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Electronic address: ksj85@kongju.ac.kr.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Biological Sciences, College of Natural Sciences, Kongju National University, Gongju</wicri:regionArea><wicri:noRegion>Gongju</wicri:noRegion></affiliation></author></analytic><series><title level="j">International journal of biological macromolecules</title><idno type="eISSN">1879-0003</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Cartilage, Articular (cytology)</term><term>Cartilage, Articular (drug effects)</term><term>Cell Dedifferentiation (drug effects)</term><term>Cell Differentiation (drug effects)</term><term>Chondrocytes (cytology)</term><term>Chondrocytes (drug effects)</term><term>Chromones (pharmacology)</term><term>Cysteamine (analogs & derivatives)</term><term>Cysteamine (chemistry)</term><term>Endoplasmic Reticulum Stress (drug effects)</term><term>Glutaredoxins (chemistry)</term><term>Glutaredoxins (genetics)</term><term>Imidazoles (pharmacology)</term><term>MAP Kinase Signaling System (drug effects)</term><term>Morpholines (pharmacology)</term><term>Peptides (chemistry)</term><term>Peptides (genetics)</term><term>Phosphatidylinositol 3-Kinases (chemistry)</term><term>Phosphatidylinositol 3-Kinases (genetics)</term><term>Pyridines (pharmacology)</term><term>Rabbits (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>4H-1-Benzopyran-4-ones (pharmacologie)</term><term>Animaux (MeSH)</term><term>Cartilage articulaire (cytologie)</term><term>Cartilage articulaire (effets des médicaments et des substances chimiques)</term><term>Chondrocytes (cytologie)</term><term>Chondrocytes (effets des médicaments et des substances chimiques)</term><term>Différenciation cellulaire (effets des médicaments et des substances chimiques)</term><term>Dédifférenciation cellulaire (effets des médicaments et des substances chimiques)</term><term>Glutarédoxines (composition chimique)</term><term>Glutarédoxines (génétique)</term><term>Imidazoles (pharmacologie)</term><term>Lapins (MeSH)</term><term>Mercaptamine (analogues et dérivés)</term><term>Mercaptamine (composition chimique)</term><term>Morpholines (pharmacologie)</term><term>Peptides (composition chimique)</term><term>Peptides (génétique)</term><term>Phosphatidylinositol 3-kinases (composition chimique)</term><term>Phosphatidylinositol 3-kinases (génétique)</term><term>Pyridines (pharmacologie)</term><term>Stress du réticulum endoplasmique (effets des médicaments et des substances chimiques)</term><term>Système de signalisation des MAP kinases (effets des médicaments et des substances chimiques)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Cysteamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Cysteamine</term><term>Glutaredoxins</term><term>Peptides</term><term>Phosphatidylinositol 3-Kinases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Glutaredoxins</term><term>Peptides</term><term>Phosphatidylinositol 3-Kinases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Chromones</term><term>Imidazoles</term><term>Morpholines</term><term>Pyridines</term></keywords><keywords scheme="MESH" qualifier="analogues et dérivés" xml:lang="fr"><term>Mercaptamine</term></keywords><keywords scheme="MESH" qualifier="composition chimique" xml:lang="fr"><term>Glutarédoxines</term><term>Mercaptamine</term><term>Peptides</term><term>Phosphatidylinositol 3-kinases</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Cartilage articulaire</term><term>Chondrocytes</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Cartilage, Articular</term><term>Chondrocytes</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cartilage, Articular</term><term>Cell Dedifferentiation</term><term>Cell Differentiation</term><term>Chondrocytes</term><term>Endoplasmic Reticulum Stress</term><term>MAP Kinase Signaling System</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Cartilage articulaire</term><term>Chondrocytes</term><term>Différenciation cellulaire</term><term>Dédifférenciation cellulaire</term><term>Stress du réticulum endoplasmique</term><term>Système de signalisation des MAP kinases</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Glutarédoxines</term><term>Peptides</term><term>Phosphatidylinositol 3-kinases</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>4H-1-Benzopyran-4-ones</term><term>Imidazoles</term><term>Morpholines</term><term>Pyridines</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Rabbits</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Lapins</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Glutaredoxin-1 (GRX-1), belonging to the oxidoreductase family, is a component of the endogenous antioxidant defense system. In this study, we evaluated the effects of PEP-1-GRX-1 in rabbit articular chondrocytes. We found that PEP-1-GRX-1 causes a loss of the differentiated chondrocyte phenotype. PEP-1-GRX-1-treated cells exhibited decreases in type II collagen expression and sulfated-proteoglycan synthesis in a dose- and time-dependent manner. PEP-1-GRX-1 causes endoplasmic reticulum (ER)-stress, as evidenced by increases in ER stress marker proteins, i.e., glucose-regulated protein (GRP) 78, GRP 94, and phospho-eukaryotic initiation factor 2 (eIF2) α. These effects were inhibited by ER stress inhibitors. PEP-1-GRX-1 increased the phosphorylation of Akt, extracellular signal-regulated kinase (ERK)-1/2, and p38. Inhibition of ERK-1/2 by PD98059 prevented PEP-1-GRX-1-induced dedifferentiation and inhibited ER stress. The blockage of PI-3K/Akt or p38 kinase with SB203580 and LY294002 accelerated PEP-1-GRX-1-induced dedifferentiation, but did not have any effect on PEP-GRX-1-induced ER stress. Our results indicate that the ERK-1/2 pathway mediates chondrocyte dedifferentiation by PEP-GRX-1-induced ER stress. The PI-3K and p38 kinase pathways regulate PEP-1-GRX-1-induced chondrocyte dedifferentiation by an ER stress-independent pathway.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29366902</PMID><DateCompleted><Year>2018</Year><Month>08</Month><Day>31</Day></DateCompleted><DateRevised><Year>2018</Year><Month>08</Month><Day>31</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1879-0003</ISSN><JournalIssue CitedMedium="Internet"><Volume>111</Volume><PubDate><Year>2018</Year><Month>May</Month></PubDate></JournalIssue><Title>International journal of biological macromolecules</Title><ISOAbbreviation>Int J Biol Macromol</ISOAbbreviation></Journal><ArticleTitle>PEP-1-glutaredoxin-1 induces dedifferentiation of rabbit articular chondrocytes by the endoplasmic reticulum stress-dependent ERK-1/2 pathway and the endoplasmic reticulum stress-independent p38 kinase and PI-3 kinase pathways.</ArticleTitle><Pagination><MedlinePgn>1059-1066</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0141-8130(17)34209-5</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.ijbiomac.2018.01.127</ELocationID><Abstract><AbstractText>Glutaredoxin-1 (GRX-1), belonging to the oxidoreductase family, is a component of the endogenous antioxidant defense system. In this study, we evaluated the effects of PEP-1-GRX-1 in rabbit articular chondrocytes. We found that PEP-1-GRX-1 causes a loss of the differentiated chondrocyte phenotype. PEP-1-GRX-1-treated cells exhibited decreases in type II collagen expression and sulfated-proteoglycan synthesis in a dose- and time-dependent manner. PEP-1-GRX-1 causes endoplasmic reticulum (ER)-stress, as evidenced by increases in ER stress marker proteins, i.e., glucose-regulated protein (GRP) 78, GRP 94, and phospho-eukaryotic initiation factor 2 (eIF2) α. These effects were inhibited by ER stress inhibitors. PEP-1-GRX-1 increased the phosphorylation of Akt, extracellular signal-regulated kinase (ERK)-1/2, and p38. Inhibition of ERK-1/2 by PD98059 prevented PEP-1-GRX-1-induced dedifferentiation and inhibited ER stress. The blockage of PI-3K/Akt or p38 kinase with SB203580 and LY294002 accelerated PEP-1-GRX-1-induced dedifferentiation, but did not have any effect on PEP-GRX-1-induced ER stress. Our results indicate that the ERK-1/2 pathway mediates chondrocyte dedifferentiation by PEP-GRX-1-induced ER stress. The PI-3K and p38 kinase pathways regulate PEP-1-GRX-1-induced chondrocyte dedifferentiation by an ER stress-independent pathway.</AbstractText><CopyrightInformation>Copyright © 2018 Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Yu</LastName><ForeName>Seon-Mi</ForeName><Initials>SM</Initials><AffiliationInfo><Affiliation>Department of Biological Sciences, College of Natural Sciences, Kongju National University, Gongju, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Choi</LastName><ForeName>Yeon Joo</ForeName><Initials>YJ</Initials><AffiliationInfo><Affiliation>Department of Biomedical Science, Research Institute of Bioscience and Biotechnology, Hallym University, Chunchon, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Song Ja</ForeName><Initials>SJ</Initials><AffiliationInfo><Affiliation>Department of Biological Sciences, College of Natural Sciences, Kongju National University, Gongju, Republic of Korea. Electronic address: ksj85@kongju.ac.kr.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2018</Year><Month>01</Month><Day>31</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Int J Biol Macromol</MedlineTA><NlmUniqueID>7909578</NlmUniqueID><ISSNLinking>0141-8130</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D002867">Chromones</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007093">Imidazoles</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009025">Morpholines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C503924">Pep-1 peptide</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010455">Peptides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011725">Pyridines</NameOfSubstance></Chemical><Chemical><RegistryNumber>31M2U1DVID</RegistryNumber><NameOfSubstance UI="C085911">2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one</NameOfSubstance></Chemical><Chemical><RegistryNumber>5UX2SD1KE2</RegistryNumber><NameOfSubstance UI="D003543">Cysteamine</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.-</RegistryNumber><NameOfSubstance UI="D019869">Phosphatidylinositol 3-Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>OU13V1EYWQ</RegistryNumber><NameOfSubstance UI="C093642">SB 203580</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002358" MajorTopicYN="N">Cartilage, Articular</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054337" MajorTopicYN="N">Cell Dedifferentiation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002454" MajorTopicYN="N">Cell Differentiation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019902" MajorTopicYN="N">Chondrocytes</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002867" MajorTopicYN="N">Chromones</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003543" MajorTopicYN="N">Cysteamine</DescriptorName><QualifierName UI="Q000031" MajorTopicYN="Y">analogs & derivatives</QualifierName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D059865" MajorTopicYN="N">Endoplasmic Reticulum Stress</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007093" MajorTopicYN="N">Imidazoles</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020935" MajorTopicYN="N">MAP Kinase Signaling System</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009025" MajorTopicYN="N">Morpholines</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010455" MajorTopicYN="N">Peptides</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019869" MajorTopicYN="N">Phosphatidylinositol 3-Kinases</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011725" MajorTopicYN="N">Pyridines</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011817" MajorTopicYN="N">Rabbits</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Chondrocytes</Keyword><Keyword MajorTopicYN="N">Dedifferentiation</Keyword><Keyword MajorTopicYN="N">Endoplasmic reticulum stress</Keyword><Keyword MajorTopicYN="N">Glutaredoxin-1</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2017</Year><Month>10</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2018</Year><Month>01</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2018</Year><Month>01</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2018</Year><Month>1</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2018</Year><Month>9</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2018</Year><Month>1</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">29366902</ArticleId><ArticleId IdType="pii">S0141-8130(17)34209-5</ArticleId><ArticleId IdType="doi">10.1016/j.ijbiomac.2018.01.127</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Corée du Sud</li></country></list><tree><country name="Corée du Sud"><noRegion><name sortKey="Yu, Seon Mi" sort="Yu, Seon Mi" uniqKey="Yu S" first="Seon-Mi" last="Yu">Seon-Mi Yu</name></noRegion><name sortKey="Choi, Yeon Joo" sort="Choi, Yeon Joo" uniqKey="Choi Y" first="Yeon Joo" last="Choi">Yeon Joo Choi</name><name sortKey="Kim, Song Ja" sort="Kim, Song Ja" uniqKey="Kim S" first="Song Ja" last="Kim">Song Ja Kim</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:29366902" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \
| NlmPubMed2Wicri -a GlutaredoxinV1
| This area was generated with Dilib version V0.6.37. |  |