Glucose uptake via glucose transporter 3 by human platelets is regulated by protein kinase B.
Identifieur interne : 003417 ( Main/Exploration ); précédent : 003416; suivant : 003418Glucose uptake via glucose transporter 3 by human platelets is regulated by protein kinase B.
Auteurs : Irlando Andrade Ferreira ; Astrid I M. Mocking ; Rolf T. Urbanus ; Samantha Varlack ; Monika Wnuk ; Jan-Willem N. AkkermanSource :
- The Journal of biological chemistry [ 0021-9258 ] ; 2005.
Descripteurs français
- KwdFr :
- ARN messager (métabolisme), Agrégation plaquettaire (MeSH), Antienzymes (pharmacologie), Azépines (métabolisme), Azépines (pharmacologie), Calcium (métabolisme), Cinétique (MeSH), Cytométrie en flux (MeSH), Facteurs temps (MeSH), Glucose (métabolisme), Glucose (pharmacocinétique), Humains (MeSH), Immunotransfert (MeSH), Insuline (métabolisme), Membrane cellulaire (métabolisme), Modèles biologiques (MeSH), Mégacaryocytes (métabolisme), Phosphorylation (MeSH), Plaquettes (enzymologie), Plaquettes (métabolisme), RT-PCR (MeSH), Relation dose-effet des médicaments (MeSH), Sélectine P (métabolisme), Sérine (composition chimique), Thrombine (métabolisme), Thrombine (pharmacologie), Transport biologique (MeSH).
- MESH :
- composition chimique : Sérine.
- enzymologie : Plaquettes.
- métabolisme : ARN messager, Azépines, Calcium, Glucose, Insuline, Membrane cellulaire, Mégacaryocytes, Plaquettes, Sélectine P, Thrombine.
- pharmacocinétique : Glucose.
- pharmacologie : Antienzymes, Azépines, Thrombine.
- Agrégation plaquettaire, Cinétique, Cytométrie en flux, Facteurs temps, Humains, Immunotransfert, Modèles biologiques, Phosphorylation, RT-PCR, Relation dose-effet des médicaments, Transport biologique.
English descriptors
- KwdEn :
- Azepines (metabolism), Azepines (pharmacology), Biological Transport (MeSH), Blood Platelets (enzymology), Blood Platelets (metabolism), Calcium (metabolism), Cell Membrane (metabolism), Dose-Response Relationship, Drug (MeSH), Enzyme Inhibitors (pharmacology), Flow Cytometry (MeSH), Glucose (metabolism), Glucose (pharmacokinetics), Humans (MeSH), Immunoblotting (MeSH), Insulin (metabolism), Kinetics (MeSH), Megakaryocytes (metabolism), Models, Biological (MeSH), P-Selectin (metabolism), Phosphorylation (MeSH), Platelet Aggregation (MeSH), RNA, Messenger (metabolism), Reverse Transcriptase Polymerase Chain Reaction (MeSH), Serine (chemistry), Thrombin (metabolism), Thrombin (pharmacology), Time Factors (MeSH).
- MESH :
- chemical , chemistry : Serine.
- chemical , metabolism : Azepines, Calcium, Glucose, Insulin, P-Selectin, RNA, Messenger, Thrombin.
- chemical , pharmacokinetics : Glucose.
- chemical , pharmacology : Azepines, Enzyme Inhibitors, Thrombin.
- enzymology : Blood Platelets.
- metabolism : Blood Platelets, Cell Membrane, Megakaryocytes.
- Biological Transport, Dose-Response Relationship, Drug, Flow Cytometry, Humans, Immunoblotting, Kinetics, Models, Biological, Phosphorylation, Platelet Aggregation, Reverse Transcriptase Polymerase Chain Reaction, Time Factors.
Abstract
In insulin-responsive tissues, insulin is a potent activator of protein kinase B (PKB)-mediated glucose uptake through the facilitative glucose transporter GLUT4. In platelets, glucose uptake is mediated through GLUT3, which is present in plasma (15%) and intracellular alpha-granule (85%) membranes. Here we report the PKB-mediated glucose uptake by platelets by agents that do (thrombin) or do not (insulin) induce alpha-granule translocation to the plasma membrane. Both thrombin and insulin activate PKB and induce glucose uptake albeit with different kinetics. Inhibition of PKB by the pharmacological inhibitor ML-9 decreases thrombin-induced alpha-granule release and thrombin- and insulin-induced glucose uptake. At low glucose (0.1 mm), both agents stimulate glucose uptake by lowering the Km for glucose (thrombin and insulin) and increasing Vmax (thrombin). At high glucose (5 mm), stimulation of glucose uptake by insulin disappears, and insulin becomes an inhibitor of thrombin-induced glucose uptake via mechanisms independent of PKB. We conclude that in platelets glucose transport through GLUT3 is regulated by changes in surface expression and affinity modulation, which are both under control of PKB.
DOI: 10.1074/jbc.M507221200
PubMed: 16049004
Affiliations:
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Urbanus</name></author><author><name sortKey="Varlack, Samantha" sort="Varlack, Samantha" uniqKey="Varlack S" first="Samantha" last="Varlack">Samantha Varlack</name></author><author><name sortKey="Wnuk, Monika" sort="Wnuk, Monika" uniqKey="Wnuk M" first="Monika" last="Wnuk">Monika Wnuk</name></author><author><name sortKey="Akkerman, Jan Willem N" sort="Akkerman, Jan Willem N" uniqKey="Akkerman J" first="Jan-Willem N" last="Akkerman">Jan-Willem N. Akkerman</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2005">2005</date><idno type="RBID">pubmed:16049004</idno><idno type="pmid">16049004</idno><idno type="doi">10.1074/jbc.M507221200</idno><idno type="wicri:Area/Main/Corpus">003375</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">003375</idno><idno type="wicri:Area/Main/Curation">003375</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">003375</idno><idno type="wicri:Area/Main/Exploration">003375</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Glucose uptake via glucose transporter 3 by human platelets is regulated by protein kinase B.</title><author><name sortKey="Ferreira, Irlando Andrade" sort="Ferreira, Irlando Andrade" uniqKey="Ferreira I" first="Irlando Andrade" last="Ferreira">Irlando Andrade Ferreira</name><affiliation><nlm:affiliation>Thrombosis and Haemostasis Laboratory, Department of Hematology, University Medical Center Utrecht.</nlm:affiliation><wicri:noCountry code="subField">University Medical Center Utrecht</wicri:noCountry></affiliation></author><author><name sortKey="Mocking, Astrid I M" sort="Mocking, Astrid I M" uniqKey="Mocking A" first="Astrid I M" last="Mocking">Astrid I M. Mocking</name></author><author><name sortKey="Urbanus, Rolf T" sort="Urbanus, Rolf T" uniqKey="Urbanus R" first="Rolf T" last="Urbanus">Rolf T. Urbanus</name></author><author><name sortKey="Varlack, Samantha" sort="Varlack, Samantha" uniqKey="Varlack S" first="Samantha" last="Varlack">Samantha Varlack</name></author><author><name sortKey="Wnuk, Monika" sort="Wnuk, Monika" uniqKey="Wnuk M" first="Monika" last="Wnuk">Monika Wnuk</name></author><author><name sortKey="Akkerman, Jan Willem N" sort="Akkerman, Jan Willem N" uniqKey="Akkerman J" first="Jan-Willem N" last="Akkerman">Jan-Willem N. Akkerman</name></author></analytic><series><title level="j">The Journal of biological chemistry</title><idno type="ISSN">0021-9258</idno><imprint><date when="2005" type="published">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Azepines (metabolism)</term><term>Azepines (pharmacology)</term><term>Biological Transport (MeSH)</term><term>Blood Platelets (enzymology)</term><term>Blood Platelets (metabolism)</term><term>Calcium (metabolism)</term><term>Cell Membrane (metabolism)</term><term>Dose-Response Relationship, Drug (MeSH)</term><term>Enzyme Inhibitors (pharmacology)</term><term>Flow Cytometry (MeSH)</term><term>Glucose (metabolism)</term><term>Glucose (pharmacokinetics)</term><term>Humans (MeSH)</term><term>Immunoblotting (MeSH)</term><term>Insulin (metabolism)</term><term>Kinetics (MeSH)</term><term>Megakaryocytes (metabolism)</term><term>Models, Biological (MeSH)</term><term>P-Selectin (metabolism)</term><term>Phosphorylation (MeSH)</term><term>Platelet Aggregation (MeSH)</term><term>RNA, Messenger (metabolism)</term><term>Reverse Transcriptase Polymerase Chain Reaction (MeSH)</term><term>Serine (chemistry)</term><term>Thrombin (metabolism)</term><term>Thrombin (pharmacology)</term><term>Time Factors (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ARN messager (métabolisme)</term><term>Agrégation plaquettaire (MeSH)</term><term>Antienzymes (pharmacologie)</term><term>Azépines (métabolisme)</term><term>Azépines (pharmacologie)</term><term>Calcium (métabolisme)</term><term>Cinétique (MeSH)</term><term>Cytométrie en flux (MeSH)</term><term>Facteurs temps (MeSH)</term><term>Glucose (métabolisme)</term><term>Glucose (pharmacocinétique)</term><term>Humains (MeSH)</term><term>Immunotransfert (MeSH)</term><term>Insuline (métabolisme)</term><term>Membrane cellulaire (métabolisme)</term><term>Modèles biologiques (MeSH)</term><term>Mégacaryocytes (métabolisme)</term><term>Phosphorylation (MeSH)</term><term>Plaquettes (enzymologie)</term><term>Plaquettes (métabolisme)</term><term>RT-PCR (MeSH)</term><term>Relation dose-effet des médicaments (MeSH)</term><term>Sélectine P (métabolisme)</term><term>Sérine (composition chimique)</term><term>Thrombine (métabolisme)</term><term>Thrombine (pharmacologie)</term><term>Transport biologique (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Serine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Azepines</term><term>Calcium</term><term>Glucose</term><term>Insulin</term><term>P-Selectin</term><term>RNA, Messenger</term><term>Thrombin</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacokinetics" xml:lang="en"><term>Glucose</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Azepines</term><term>Enzyme Inhibitors</term><term>Thrombin</term></keywords><keywords scheme="MESH" qualifier="composition chimique" xml:lang="fr"><term>Sérine</term></keywords><keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Plaquettes</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Blood Platelets</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Blood Platelets</term><term>Cell Membrane</term><term>Megakaryocytes</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>ARN messager</term><term>Azépines</term><term>Calcium</term><term>Glucose</term><term>Insuline</term><term>Membrane cellulaire</term><term>Mégacaryocytes</term><term>Plaquettes</term><term>Sélectine P</term><term>Thrombine</term></keywords><keywords scheme="MESH" qualifier="pharmacocinétique" xml:lang="fr"><term>Glucose</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antienzymes</term><term>Azépines</term><term>Thrombine</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Biological Transport</term><term>Dose-Response Relationship, Drug</term><term>Flow Cytometry</term><term>Humans</term><term>Immunoblotting</term><term>Kinetics</term><term>Models, Biological</term><term>Phosphorylation</term><term>Platelet Aggregation</term><term>Reverse Transcriptase Polymerase Chain Reaction</term><term>Time Factors</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Agrégation plaquettaire</term><term>Cinétique</term><term>Cytométrie en flux</term><term>Facteurs temps</term><term>Humains</term><term>Immunotransfert</term><term>Modèles biologiques</term><term>Phosphorylation</term><term>RT-PCR</term><term>Relation dose-effet des médicaments</term><term>Transport biologique</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In insulin-responsive tissues, insulin is a potent activator of protein kinase B (PKB)-mediated glucose uptake through the facilitative glucose transporter GLUT4. In platelets, glucose uptake is mediated through GLUT3, which is present in plasma (15%) and intracellular alpha-granule (85%) membranes. Here we report the PKB-mediated glucose uptake by platelets by agents that do (thrombin) or do not (insulin) induce alpha-granule translocation to the plasma membrane. Both thrombin and insulin activate PKB and induce glucose uptake albeit with different kinetics. Inhibition of PKB by the pharmacological inhibitor ML-9 decreases thrombin-induced alpha-granule release and thrombin- and insulin-induced glucose uptake. At low glucose (0.1 mm), both agents stimulate glucose uptake by lowering the Km for glucose (thrombin and insulin) and increasing Vmax (thrombin). At high glucose (5 mm), stimulation of glucose uptake by insulin disappears, and insulin becomes an inhibitor of thrombin-induced glucose uptake via mechanisms independent of PKB. We conclude that in platelets glucose transport through GLUT3 is regulated by changes in surface expression and affinity modulation, which are both under control of PKB.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16049004</PMID><DateCompleted><Year>2005</Year><Month>11</Month><Day>28</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0021-9258</ISSN><JournalIssue CitedMedium="Print"><Volume>280</Volume><Issue>38</Issue><PubDate><Year>2005</Year><Month>Sep</Month><Day>23</Day></PubDate></JournalIssue><Title>The Journal of biological chemistry</Title><ISOAbbreviation>J Biol Chem</ISOAbbreviation></Journal><ArticleTitle>Glucose uptake via glucose transporter 3 by human platelets is regulated by protein kinase B.</ArticleTitle><Pagination><MedlinePgn>32625-33</MedlinePgn></Pagination><Abstract><AbstractText>In insulin-responsive tissues, insulin is a potent activator of protein kinase B (PKB)-mediated glucose uptake through the facilitative glucose transporter GLUT4. In platelets, glucose uptake is mediated through GLUT3, which is present in plasma (15%) and intracellular alpha-granule (85%) membranes. Here we report the PKB-mediated glucose uptake by platelets by agents that do (thrombin) or do not (insulin) induce alpha-granule translocation to the plasma membrane. Both thrombin and insulin activate PKB and induce glucose uptake albeit with different kinetics. Inhibition of PKB by the pharmacological inhibitor ML-9 decreases thrombin-induced alpha-granule release and thrombin- and insulin-induced glucose uptake. At low glucose (0.1 mm), both agents stimulate glucose uptake by lowering the Km for glucose (thrombin and insulin) and increasing Vmax (thrombin). At high glucose (5 mm), stimulation of glucose uptake by insulin disappears, and insulin becomes an inhibitor of thrombin-induced glucose uptake via mechanisms independent of PKB. We conclude that in platelets glucose transport through GLUT3 is regulated by changes in surface expression and affinity modulation, which are both under control of PKB.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ferreira</LastName><ForeName>Irlando Andrade</ForeName><Initials>IA</Initials><AffiliationInfo><Affiliation>Thrombosis and Haemostasis Laboratory, Department of Hematology, University Medical Center Utrecht.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mocking</LastName><ForeName>Astrid I M</ForeName><Initials>AI</Initials></Author><Author ValidYN="Y"><LastName>Urbanus</LastName><ForeName>Rolf T</ForeName><Initials>RT</Initials></Author><Author ValidYN="Y"><LastName>Varlack</LastName><ForeName>Samantha</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Wnuk</LastName><ForeName>Monika</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Akkerman</LastName><ForeName>Jan-Willem N</ForeName><Initials>JW</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2005</Year><Month>07</Month><Day>26</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Biol Chem</MedlineTA><NlmUniqueID>2985121R</NlmUniqueID><ISSNLinking>0021-9258</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001381">Azepines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004791">Enzyme Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007328">Insulin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019007">P-Selectin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance></Chemical><Chemical><RegistryNumber>105637-50-1</RegistryNumber><NameOfSubstance UI="C056218">ML 9</NameOfSubstance></Chemical><Chemical><RegistryNumber>452VLY9402</RegistryNumber><NameOfSubstance UI="D012694">Serine</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.21.5</RegistryNumber><NameOfSubstance UI="D013917">Thrombin</NameOfSubstance></Chemical><Chemical><RegistryNumber>IY9XDZ35W2</RegistryNumber><NameOfSubstance UI="D005947">Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>SY7Q814VUP</RegistryNumber><NameOfSubstance UI="D002118">Calcium</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001381" MajorTopicYN="N">Azepines</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001692" MajorTopicYN="N">Biological Transport</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001792" MajorTopicYN="N">Blood Platelets</DescriptorName><QualifierName UI="Q000201" MajorTopicYN="Y">enzymology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002118" MajorTopicYN="N">Calcium</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002462" MajorTopicYN="N">Cell Membrane</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004305" MajorTopicYN="N">Dose-Response Relationship, Drug</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004791" MajorTopicYN="N">Enzyme Inhibitors</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005434" MajorTopicYN="N">Flow Cytometry</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005947" MajorTopicYN="N">Glucose</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000493" MajorTopicYN="Y">pharmacokinetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015151" MajorTopicYN="N">Immunoblotting</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007328" MajorTopicYN="N">Insulin</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007700" MajorTopicYN="N">Kinetics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008533" MajorTopicYN="N">Megakaryocytes</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008954" MajorTopicYN="N">Models, Biological</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019007" MajorTopicYN="N">P-Selectin</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010766" MajorTopicYN="N">Phosphorylation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010974" MajorTopicYN="N">Platelet Aggregation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012333" MajorTopicYN="N">RNA, Messenger</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020133" MajorTopicYN="N">Reverse Transcriptase Polymerase Chain Reaction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012694" MajorTopicYN="N">Serine</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013917" MajorTopicYN="N">Thrombin</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013997" MajorTopicYN="N">Time Factors</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2005</Year><Month>7</Month><Day>29</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2005</Year><Month>12</Month><Day>13</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2005</Year><Month>7</Month><Day>29</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">16049004</ArticleId><ArticleId IdType="pii">M507221200</ArticleId><ArticleId IdType="doi">10.1074/jbc.M507221200</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list></list><tree><noCountry><name sortKey="Akkerman, Jan Willem N" sort="Akkerman, Jan Willem N" uniqKey="Akkerman J" first="Jan-Willem N" last="Akkerman">Jan-Willem N. Akkerman</name><name sortKey="Ferreira, Irlando Andrade" sort="Ferreira, Irlando Andrade" uniqKey="Ferreira I" first="Irlando Andrade" last="Ferreira">Irlando Andrade Ferreira</name><name sortKey="Mocking, Astrid I M" sort="Mocking, Astrid I M" uniqKey="Mocking A" first="Astrid I M" last="Mocking">Astrid I M. Mocking</name><name sortKey="Urbanus, Rolf T" sort="Urbanus, Rolf T" uniqKey="Urbanus R" first="Rolf T" last="Urbanus">Rolf T. Urbanus</name><name sortKey="Varlack, Samantha" sort="Varlack, Samantha" uniqKey="Varlack S" first="Samantha" last="Varlack">Samantha Varlack</name><name sortKey="Wnuk, Monika" sort="Wnuk, Monika" uniqKey="Wnuk M" first="Monika" last="Wnuk">Monika Wnuk</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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