Effect of glucose concentration on activation of the ASK1-SEK1-JNK1 signal transduction pathway.
Identifieur interne : 000F42 ( Main/Exploration ); précédent : 000F41; suivant : 000F43Effect of glucose concentration on activation of the ASK1-SEK1-JNK1 signal transduction pathway.
Auteurs : Jae J. Song [États-Unis] ; Yong J. LeeSource :
- Journal of cellular biochemistry [ 0730-2312 ] ; 2003.
Descripteurs français
- KwdFr :
- Activation enzymatique (effets des médicaments et des substances chimiques), Adenoviridae (génétique), Cellules cancéreuses en culture (MeSH), Dimérisation (MeSH), Facteur-2 associé aux récepteurs de TNF (MeSH), Glucose (déficit), Glucose (pharmacologie), Glutarédoxines (MeSH), Humains (MeSH), Immunotransfert (MeSH), MAP Kinase Kinase 4 (MeSH), MAP Kinase Kinase Kinase 5 (MeSH), MAP Kinase Kinase Kinases (métabolisme), Mitogen-Activated Protein Kinase 8 (MeSH), Mitogen-Activated Protein Kinase Kinases (métabolisme), Mitogen-Activated Protein Kinases (métabolisme), Mâle (MeSH), Oxidoreductases (MeSH), Protéines (métabolisme), Protéines virales (métabolisme), Système de signalisation des MAP kinases (effets des médicaments et des substances chimiques), Thiorédoxines (métabolisme), Tumeurs de la prostate (métabolisme), Vecteurs génétiques (génétique).
- MESH :
- déficit : Glucose.
- effets des médicaments et des substances chimiques : Activation enzymatique, Système de signalisation des MAP kinases.
- génétique : Adenoviridae, Vecteurs génétiques.
- métabolisme : MAP Kinase Kinase Kinases, Mitogen-Activated Protein Kinase Kinases, Mitogen-Activated Protein Kinases, Protéines, Protéines virales, Thiorédoxines, Tumeurs de la prostate.
- pharmacologie : Glucose.
- Cellules cancéreuses en culture, Dimérisation, Facteur-2 associé aux récepteurs de TNF, Glutarédoxines, Humains, Immunotransfert, MAP Kinase Kinase 4, MAP Kinase Kinase Kinase 5, Mitogen-Activated Protein Kinase 8, Mâle, Oxidoreductases.
English descriptors
- KwdEn :
- Adenoviridae (genetics), Dimerization (MeSH), Enzyme Activation (drug effects), Genetic Vectors (genetics), Glucose (deficiency), Glucose (pharmacology), Glutaredoxins (MeSH), Humans (MeSH), Immunoblotting (MeSH), MAP Kinase Kinase 4 (MeSH), MAP Kinase Kinase Kinase 5 (MeSH), MAP Kinase Kinase Kinases (metabolism), MAP Kinase Signaling System (drug effects), Male (MeSH), Mitogen-Activated Protein Kinase 8 (MeSH), Mitogen-Activated Protein Kinase Kinases (metabolism), Mitogen-Activated Protein Kinases (metabolism), Oxidoreductases (MeSH), Prostatic Neoplasms (metabolism), Proteins (metabolism), TNF Receptor-Associated Factor 2 (MeSH), Thioredoxins (metabolism), Tumor Cells, Cultured (MeSH), Viral Proteins (metabolism).
- MESH :
- chemical , deficiency : Glucose.
- drug effects : Enzyme Activation, MAP Kinase Signaling System.
- genetics : Adenoviridae, Genetic Vectors.
- chemical , metabolism : MAP Kinase Kinase Kinases, Mitogen-Activated Protein Kinase Kinases, Mitogen-Activated Protein Kinases, Prostatic Neoplasms, Proteins, Thioredoxins, Viral Proteins.
- chemical , pharmacology : Glucose.
- Dimerization, Glutaredoxins, Humans, Immunoblotting, MAP Kinase Kinase 4, MAP Kinase Kinase Kinase 5, Male, Mitogen-Activated Protein Kinase 8, Oxidoreductases, TNF Receptor-Associated Factor 2, Tumor Cells, Cultured.
Abstract
Recently, acute total glucose deprivation has been shown to cause activation of ASK1-MEK-MAPK signal transduction and dissociation of glutaredoxin (GRX) from apoptosis signal-regulating kinase 1 (ASK1). In this study, we investigated whether clinically relevant concentrations (0.01-0.1 mM) of glucose promote ASK1 activation. We observed that a prominent activation of JNK1 occurred at a glucose concentration less than or equal to 0.01 mM. Similar to JNK1 activation, we also observed that low glucose-induced ASK1 activation, dissociation of GRX and thioredoxin (TRX) from ASK1, dimerization of ASK1, and association of Daxx and TRAF2 with ASK1 significantly occurred at a glucose concentration less than or equal to 0.01 mM.
DOI: 10.1002/jcb.10541
PubMed: 12858332
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Song</name><affiliation wicri:level="4"><nlm:affiliation>Department of Surgery, University of Pittsburgh, The Hillman Cancer Center G.5a, 5117 Centre Ave., Pittsburgh, PA 15213, USA. leeyj@msx.upmc.edu</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Surgery, University of Pittsburgh, The Hillman Cancer Center G.5a, 5117 Centre Ave., 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. 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type="abstract" xml:lang="en">Recently, acute total glucose deprivation has been shown to cause activation of ASK1-MEK-MAPK signal transduction and dissociation of glutaredoxin (GRX) from apoptosis signal-regulating kinase 1 (ASK1). In this study, we investigated whether clinically relevant concentrations (0.01-0.1 mM) of glucose promote ASK1 activation. We observed that a prominent activation of JNK1 occurred at a glucose concentration less than or equal to 0.01 mM. Similar to JNK1 activation, we also observed that low glucose-induced ASK1 activation, dissociation of GRX and thioredoxin (TRX) from ASK1, dimerization of ASK1, and association of Daxx and TRAF2 with ASK1 significantly occurred at a glucose concentration less than or equal to 0.01 mM.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">12858332</PMID><DateCompleted><Year>2003</Year><Month>11</Month><Day>17</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>24</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0730-2312</ISSN><JournalIssue CitedMedium="Print"><Volume>89</Volume><Issue>4</Issue><PubDate><Year>2003</Year><Month>Jul</Month><Day>01</Day></PubDate></JournalIssue><Title>Journal of cellular biochemistry</Title><ISOAbbreviation>J Cell Biochem</ISOAbbreviation></Journal><ArticleTitle>Effect of glucose concentration on activation of the ASK1-SEK1-JNK1 signal transduction pathway.</ArticleTitle><Pagination><MedlinePgn>653-62</MedlinePgn></Pagination><Abstract><AbstractText>Recently, acute total glucose deprivation has been shown to cause activation of ASK1-MEK-MAPK signal transduction and dissociation of glutaredoxin (GRX) from apoptosis signal-regulating kinase 1 (ASK1). In this study, we investigated whether clinically relevant concentrations (0.01-0.1 mM) of glucose promote ASK1 activation. We observed that a prominent activation of JNK1 occurred at a glucose concentration less than or equal to 0.01 mM. Similar to JNK1 activation, we also observed that low glucose-induced ASK1 activation, dissociation of GRX and thioredoxin (TRX) from ASK1, dimerization of ASK1, and association of Daxx and TRAF2 with ASK1 significantly occurred at a glucose concentration less than or equal to 0.01 mM.</AbstractText><CopyrightInformation>Copyright 2003 Wiley-Liss, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Song</LastName><ForeName>Jae J</ForeName><Initials>JJ</Initials><AffiliationInfo><Affiliation>Department of Surgery, University of Pittsburgh, The Hillman Cancer Center G.5a, 5117 Centre Ave., Pittsburgh, PA 15213, USA. leeyj@msx.upmc.edu</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></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>United States</Country><MedlineTA>J Cell Biochem</MedlineTA><NlmUniqueID>8205768</NlmUniqueID><ISSNLinking>0730-2312</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 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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>EC 2.7.12.2</RegistryNumber><NameOfSubstance UI="D048670">MAP Kinase Kinase 4</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.12.2</RegistryNumber><NameOfSubstance UI="C482559">MAP2K4 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.12.2</RegistryNumber><NameOfSubstance UI="D020929">Mitogen-Activated Protein Kinase Kinases</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="D019281" MajorTopicYN="N">Dimerization</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004789" MajorTopicYN="N">Enzyme Activation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005822" MajorTopicYN="N">Genetic Vectors</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005947" MajorTopicYN="N">Glucose</DescriptorName><QualifierName UI="Q000172" MajorTopicYN="N">deficiency</QualifierName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" 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PubStatus="entrez"><Year>2003</Year><Month>7</Month><Day>15</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">12858332</ArticleId><ArticleId IdType="doi">10.1002/jcb.10541</ArticleId></ArticleIdList></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)
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