Role of the JNK pathway in NMDA-mediated excitotoxicity of cortical neurons
Excitotoxic insults induce c-Jun N-terminal kinase (JNK) activation, which leads to neuronal death and contributes to many neurological conditions such as cerebral ischemia and neurodegenerative disorders. The action of JNK can be inhibited by the D - retro-inverso form of JNK inhibitor peptide (D-J...
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| Veröffentlicht in: | Cell death and differentiation 2007-02, Vol.14 (2), p.240-253 |
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| creator | Centeno, C Repici, M Chatton, J-Y Riederer, B M Bonny, C Nicod, P Price, M Clarke, P G H Papa, S Franzoso, G Borsello, T |
| description | Excitotoxic insults induce c-Jun N-terminal kinase (JNK) activation, which leads to neuronal death and contributes to many neurological conditions such as cerebral ischemia and neurodegenerative disorders. The action of JNK can be inhibited by the
D
-
retro-inverso
form of JNK inhibitor peptide (D-JNKI1), which totally prevents death induced by N-methyl-
D
-aspartate (NMDA)
in vitro
and strongly protects against different
in vivo
paradigms of excitotoxicity. To obtain optimal neuroprotection, it is imperative to elucidate the prosurvival action of D-JNKI1 and the death pathways that it inhibits. In cortical neuronal cultures, we first investigate the pathways by which NMDA induces JNK activation and show a rapid and selective phosphorylation of mitogen-activated protein kinase kinase 7 (MKK7), whereas the only other known JNK activator, mitogen-activated protein kinase kinase 4 (MKK4), was unaffected. We then analyze the action of D-JNKI1 on four JNK targets containing a JNK-binding domain:
M
APK-
a
ctivating
d
eath
d
omain-containing protein/
d
ifferentially
e
xpressed in
n
ormal and
n
eoplastic cells (MADD/DENN), MKK7, MKK4 and JNK-interacting protein-1 (IB1/JIP-1). |
| doi_str_mv | 10.1038/sj.cdd.4401988 |
| format | Article |
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D
-
retro-inverso
form of JNK inhibitor peptide (D-JNKI1), which totally prevents death induced by N-methyl-
D
-aspartate (NMDA)
in vitro
and strongly protects against different
in vivo
paradigms of excitotoxicity. To obtain optimal neuroprotection, it is imperative to elucidate the prosurvival action of D-JNKI1 and the death pathways that it inhibits. In cortical neuronal cultures, we first investigate the pathways by which NMDA induces JNK activation and show a rapid and selective phosphorylation of mitogen-activated protein kinase kinase 7 (MKK7), whereas the only other known JNK activator, mitogen-activated protein kinase kinase 4 (MKK4), was unaffected. We then analyze the action of D-JNKI1 on four JNK targets containing a JNK-binding domain:
M
APK-
a
ctivating
d
eath
d
omain-containing protein/
d
ifferentially
e
xpressed in
n
ormal and
n
eoplastic cells (MADD/DENN), MKK7, MKK4 and JNK-interacting protein-1 (IB1/JIP-1).</description><identifier>ISSN: 1350-9047</identifier><identifier>EISSN: 1476-5403</identifier><identifier>DOI: 10.1038/sj.cdd.4401988</identifier><identifier>PMID: 16794604</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Adaptor Proteins, Signal Transducing - isolation & purification ; Adaptor Proteins, Signal Transducing - metabolism ; Animals ; Apoptosis ; Biochemistry ; Biomedical and Life Sciences ; Calcium - metabolism ; Cell Biology ; Cell Cycle Analysis ; Cell death ; Cerebral Cortex - cytology ; Cerebral Cortex - drug effects ; Cerebral Cortex - enzymology ; Cycloheximide - pharmacology ; Death Domain Receptor Signaling Adaptor Proteins ; Electrophoresis, Gel, Two-Dimensional ; Enzyme Activation - drug effects ; Enzyme Inhibitors - pharmacology ; Fluorescent Antibody Technique ; Guanine Nucleotide Exchange Factors - metabolism ; Ischemia ; JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors ; JNK Mitogen-Activated Protein Kinases - metabolism ; Kinases ; Life Sciences ; MAP Kinase Kinase 4 - metabolism ; MAP Kinase Kinase 7 - metabolism ; Microscopy ; N-Methylaspartate - toxicity ; Neurodegeneration ; Neurons - cytology ; Neurons - drug effects ; Neurons - enzymology ; Neurons - pathology ; Neurotoxins - toxicity ; original-paper ; Peptides ; Phosphorylation - drug effects ; Proteins ; Proteomics ; Rats ; Signal transduction ; Signal Transduction - drug effects ; Stem Cells</subject><ispartof>Cell death and differentiation, 2007-02, Vol.14 (2), p.240-253</ispartof><rights>Springer Nature Limited 2007</rights><rights>Copyright Nature Publishing Group Feb 2007</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c497t-d33ddca09c88c0f12f21ac5b83c6ffe5214ca5f6563d76873c2ecef300b2856f3</citedby><cites>FETCH-LOGICAL-c497t-d33ddca09c88c0f12f21ac5b83c6ffe5214ca5f6563d76873c2ecef300b2856f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/sj.cdd.4401988$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/sj.cdd.4401988$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16794604$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Centeno, C</creatorcontrib><creatorcontrib>Repici, M</creatorcontrib><creatorcontrib>Chatton, J-Y</creatorcontrib><creatorcontrib>Riederer, B M</creatorcontrib><creatorcontrib>Bonny, C</creatorcontrib><creatorcontrib>Nicod, P</creatorcontrib><creatorcontrib>Price, M</creatorcontrib><creatorcontrib>Clarke, P G H</creatorcontrib><creatorcontrib>Papa, S</creatorcontrib><creatorcontrib>Franzoso, G</creatorcontrib><creatorcontrib>Borsello, T</creatorcontrib><title>Role of the JNK pathway in NMDA-mediated excitotoxicity of cortical neurons</title><title>Cell death and differentiation</title><addtitle>Cell Death Differ</addtitle><addtitle>Cell Death Differ</addtitle><description>Excitotoxic insults induce c-Jun N-terminal kinase (JNK) activation, which leads to neuronal death and contributes to many neurological conditions such as cerebral ischemia and neurodegenerative disorders. The action of JNK can be inhibited by the
D
-
retro-inverso
form of JNK inhibitor peptide (D-JNKI1), which totally prevents death induced by N-methyl-
D
-aspartate (NMDA)
in vitro
and strongly protects against different
in vivo
paradigms of excitotoxicity. To obtain optimal neuroprotection, it is imperative to elucidate the prosurvival action of D-JNKI1 and the death pathways that it inhibits. In cortical neuronal cultures, we first investigate the pathways by which NMDA induces JNK activation and show a rapid and selective phosphorylation of mitogen-activated protein kinase kinase 7 (MKK7), whereas the only other known JNK activator, mitogen-activated protein kinase kinase 4 (MKK4), was unaffected. We then analyze the action of D-JNKI1 on four JNK targets containing a JNK-binding domain:
M
APK-
a
ctivating
d
eath
d
omain-containing protein/
d
ifferentially
e
xpressed in
n
ormal and
n
eoplastic cells (MADD/DENN), MKK7, MKK4 and JNK-interacting protein-1 (IB1/JIP-1).</description><subject>Adaptor Proteins, Signal Transducing - isolation & purification</subject><subject>Adaptor Proteins, Signal Transducing - metabolism</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Calcium - metabolism</subject><subject>Cell Biology</subject><subject>Cell Cycle Analysis</subject><subject>Cell death</subject><subject>Cerebral Cortex - cytology</subject><subject>Cerebral Cortex - drug effects</subject><subject>Cerebral Cortex - enzymology</subject><subject>Cycloheximide - pharmacology</subject><subject>Death Domain Receptor Signaling Adaptor Proteins</subject><subject>Electrophoresis, Gel, Two-Dimensional</subject><subject>Enzyme Activation - drug effects</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Fluorescent Antibody Technique</subject><subject>Guanine Nucleotide Exchange Factors - metabolism</subject><subject>Ischemia</subject><subject>JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors</subject><subject>JNK Mitogen-Activated Protein Kinases - metabolism</subject><subject>Kinases</subject><subject>Life Sciences</subject><subject>MAP Kinase Kinase 4 - metabolism</subject><subject>MAP Kinase Kinase 7 - metabolism</subject><subject>Microscopy</subject><subject>N-Methylaspartate - toxicity</subject><subject>Neurodegeneration</subject><subject>Neurons - cytology</subject><subject>Neurons - drug effects</subject><subject>Neurons - enzymology</subject><subject>Neurons - pathology</subject><subject>Neurotoxins - toxicity</subject><subject>original-paper</subject><subject>Peptides</subject><subject>Phosphorylation - drug effects</subject><subject>Proteins</subject><subject>Proteomics</subject><subject>Rats</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Stem Cells</subject><issn>1350-9047</issn><issn>1476-5403</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kEtLAzEURoMoPqpblzK4cDf1ZvKcZalvawXRdUgziU6ZTmoyg_bfm9KCILj6Avfc74aD0CmGIQYiL-N8aKpqSCngUsoddIip4DmjQHbTmzDIS6DiAB3FOAcALkq-jw5wSsqBHqLHF9_YzLus-7DZw_QxW-ru40uvsrrNpk9Xo3xhq1p3tsrst6k73_nvOuVqvWJ86Gqjm6y1ffBtPEZ7TjfRnmxzgN5url_Hd_nk-fZ-PJrkhpaiyytCqspoKI2UBhwuXIG1YTNJDHfOsgJTo5njjJNKcCmIKayxjgDMCsm4IwN0seldBv_Z29ipRR2NbRrdWt9HhUsmBQOSwPM_4Nz3oU1_UwUWoig48AQNN5AJPsZgnVqGeqHDSmFQa8cqzlVyrLaO08LZtrWfJTu_-FZqAi43QEyj9t2G37P_VP4AGBWHUQ</recordid><startdate>20070201</startdate><enddate>20070201</enddate><creator>Centeno, C</creator><creator>Repici, M</creator><creator>Chatton, J-Y</creator><creator>Riederer, B M</creator><creator>Bonny, C</creator><creator>Nicod, P</creator><creator>Price, M</creator><creator>Clarke, P G H</creator><creator>Papa, S</creator><creator>Franzoso, G</creator><creator>Borsello, T</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope></search><sort><creationdate>20070201</creationdate><title>Role of the JNK pathway in NMDA-mediated excitotoxicity of cortical neurons</title><author>Centeno, C ; Repici, M ; Chatton, J-Y ; Riederer, B M ; Bonny, C ; Nicod, P ; Price, M ; Clarke, P G H ; Papa, S ; Franzoso, G ; Borsello, T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c497t-d33ddca09c88c0f12f21ac5b83c6ffe5214ca5f6563d76873c2ecef300b2856f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adaptor Proteins, Signal Transducing - 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metabolism</topic><topic>MAP Kinase Kinase 7 - metabolism</topic><topic>Microscopy</topic><topic>N-Methylaspartate - toxicity</topic><topic>Neurodegeneration</topic><topic>Neurons - cytology</topic><topic>Neurons - drug effects</topic><topic>Neurons - enzymology</topic><topic>Neurons - pathology</topic><topic>Neurotoxins - toxicity</topic><topic>original-paper</topic><topic>Peptides</topic><topic>Phosphorylation - drug effects</topic><topic>Proteins</topic><topic>Proteomics</topic><topic>Rats</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Stem Cells</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Centeno, C</creatorcontrib><creatorcontrib>Repici, M</creatorcontrib><creatorcontrib>Chatton, J-Y</creatorcontrib><creatorcontrib>Riederer, B M</creatorcontrib><creatorcontrib>Bonny, C</creatorcontrib><creatorcontrib>Nicod, P</creatorcontrib><creatorcontrib>Price, M</creatorcontrib><creatorcontrib>Clarke, P G H</creatorcontrib><creatorcontrib>Papa, S</creatorcontrib><creatorcontrib>Franzoso, G</creatorcontrib><creatorcontrib>Borsello, T</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Genetics Abstracts</collection><jtitle>Cell death and differentiation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Centeno, C</au><au>Repici, M</au><au>Chatton, J-Y</au><au>Riederer, B M</au><au>Bonny, C</au><au>Nicod, P</au><au>Price, M</au><au>Clarke, P G H</au><au>Papa, S</au><au>Franzoso, G</au><au>Borsello, T</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of the JNK pathway in NMDA-mediated excitotoxicity of cortical neurons</atitle><jtitle>Cell death and differentiation</jtitle><stitle>Cell Death Differ</stitle><addtitle>Cell Death Differ</addtitle><date>2007-02-01</date><risdate>2007</risdate><volume>14</volume><issue>2</issue><spage>240</spage><epage>253</epage><pages>240-253</pages><issn>1350-9047</issn><eissn>1476-5403</eissn><abstract>Excitotoxic insults induce c-Jun N-terminal kinase (JNK) activation, which leads to neuronal death and contributes to many neurological conditions such as cerebral ischemia and neurodegenerative disorders. The action of JNK can be inhibited by the
D
-
retro-inverso
form of JNK inhibitor peptide (D-JNKI1), which totally prevents death induced by N-methyl-
D
-aspartate (NMDA)
in vitro
and strongly protects against different
in vivo
paradigms of excitotoxicity. To obtain optimal neuroprotection, it is imperative to elucidate the prosurvival action of D-JNKI1 and the death pathways that it inhibits. In cortical neuronal cultures, we first investigate the pathways by which NMDA induces JNK activation and show a rapid and selective phosphorylation of mitogen-activated protein kinase kinase 7 (MKK7), whereas the only other known JNK activator, mitogen-activated protein kinase kinase 4 (MKK4), was unaffected. We then analyze the action of D-JNKI1 on four JNK targets containing a JNK-binding domain:
M
APK-
a
ctivating
d
eath
d
omain-containing protein/
d
ifferentially
e
xpressed in
n
ormal and
n
eoplastic cells (MADD/DENN), MKK7, MKK4 and JNK-interacting protein-1 (IB1/JIP-1).</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>16794604</pmid><doi>10.1038/sj.cdd.4401988</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
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| ispartof | Cell death and differentiation, 2007-02, Vol.14 (2), p.240-253 |
| issn | 1350-9047 1476-5403 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_19587503 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; SpringerLink Journals - AutoHoldings |
| subjects | Adaptor Proteins, Signal Transducing - isolation & purification Adaptor Proteins, Signal Transducing - metabolism Animals Apoptosis Biochemistry Biomedical and Life Sciences Calcium - metabolism Cell Biology Cell Cycle Analysis Cell death Cerebral Cortex - cytology Cerebral Cortex - drug effects Cerebral Cortex - enzymology Cycloheximide - pharmacology Death Domain Receptor Signaling Adaptor Proteins Electrophoresis, Gel, Two-Dimensional Enzyme Activation - drug effects Enzyme Inhibitors - pharmacology Fluorescent Antibody Technique Guanine Nucleotide Exchange Factors - metabolism Ischemia JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors JNK Mitogen-Activated Protein Kinases - metabolism Kinases Life Sciences MAP Kinase Kinase 4 - metabolism MAP Kinase Kinase 7 - metabolism Microscopy N-Methylaspartate - toxicity Neurodegeneration Neurons - cytology Neurons - drug effects Neurons - enzymology Neurons - pathology Neurotoxins - toxicity original-paper Peptides Phosphorylation - drug effects Proteins Proteomics Rats Signal transduction Signal Transduction - drug effects Stem Cells |
| title | Role of the JNK pathway in NMDA-mediated excitotoxicity of cortical neurons |
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