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Article: dp5/HRK is a c-jun target gene and required for apoptosis induced by potassium deprivation in cerebellar granule neurons

Titledp5/HRK is a c-jun target gene and required for apoptosis induced by potassium deprivation in cerebellar granule neurons
Authors
Issue Date2007
PublisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/
Citation
Journal Of Biological Chemistry, 2007, v. 282 n. 42, p. 30901-30909 How to Cite?
AbstractIn cerebellar granule neurons, a BH3-only Bcl-2 family member, death protein 5/harakiri, is up-regulated in a JNK-dependent manner during apoptosis induced by potassium deprivation. However, it is not clear whether c-Jun is directly involved in the induction of dp5. Here, we showed that the up-regulation of dp5, but not fas ligand and bim, after potassium deprivation was suppressed by the expression of a dominant negative form of c-Jun. Deletion analysis of the 5′-flanking sequence of the dp5 gene revealed that a major responsive element responsible for the induction by potassium deprivation is an ATF binding site located at -116 to -109 relative to the transcriptional start site. Mutation of this site completely abolished promoter activation. Furthermore, a gel shift assay showed that a specific complex containing c-Jun and ATF2 recognized this site and increased in potassium-deprived cerebellar granule neurons. Chromatin immunoprecipitation demonstrated that c-Jun was able to bind to this site in vivo. Finally, we demonstrated that knockdown of Dp5 by small interfering RNA rescued neurons from potassium deprivation-induced apoptosis. Taken together, these results suggest that dp5 is a target gene of c-Jun and plays a critical role in potassium deprivation-induced apoptosis in cerebellar granule neurons. © 2007 by The American Society for Biochemistry and Molecular Biology, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/149678
ISSN
2015 Impact Factor: 4.258
2015 SCImago Journal Rankings: 3.151
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMa, Cen_US
dc.contributor.authorYing, Cen_US
dc.contributor.authorYuan, Zen_US
dc.contributor.authorSong, Ben_US
dc.contributor.authorLi, Den_US
dc.contributor.authorLiu, Yen_US
dc.contributor.authorLai, Ben_US
dc.contributor.authorLi, Wen_US
dc.contributor.authorChen, Ren_US
dc.contributor.authorChing, YPen_US
dc.contributor.authorLi, Men_US
dc.date.accessioned2012-06-26T05:56:59Z-
dc.date.available2012-06-26T05:56:59Z-
dc.date.issued2007en_US
dc.identifier.citationJournal Of Biological Chemistry, 2007, v. 282 n. 42, p. 30901-30909en_US
dc.identifier.issn0021-9258en_US
dc.identifier.urihttp://hdl.handle.net/10722/149678-
dc.description.abstractIn cerebellar granule neurons, a BH3-only Bcl-2 family member, death protein 5/harakiri, is up-regulated in a JNK-dependent manner during apoptosis induced by potassium deprivation. However, it is not clear whether c-Jun is directly involved in the induction of dp5. Here, we showed that the up-regulation of dp5, but not fas ligand and bim, after potassium deprivation was suppressed by the expression of a dominant negative form of c-Jun. Deletion analysis of the 5′-flanking sequence of the dp5 gene revealed that a major responsive element responsible for the induction by potassium deprivation is an ATF binding site located at -116 to -109 relative to the transcriptional start site. Mutation of this site completely abolished promoter activation. Furthermore, a gel shift assay showed that a specific complex containing c-Jun and ATF2 recognized this site and increased in potassium-deprived cerebellar granule neurons. Chromatin immunoprecipitation demonstrated that c-Jun was able to bind to this site in vivo. Finally, we demonstrated that knockdown of Dp5 by small interfering RNA rescued neurons from potassium deprivation-induced apoptosis. Taken together, these results suggest that dp5 is a target gene of c-Jun and plays a critical role in potassium deprivation-induced apoptosis in cerebellar granule neurons. © 2007 by The American Society for Biochemistry and Molecular Biology, Inc.en_US
dc.languageengen_US
dc.publisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/en_US
dc.relation.ispartofJournal of Biological Chemistryen_US
dc.rightsJournal of Biological Chemistry. Copyright © American Society for Biochemistry and Molecular Biology, Inc.-
dc.subject.meshActivating Transcription Factor 2 - Genetics - Metabolismen_US
dc.subject.meshAnimalsen_US
dc.subject.meshApoptosis - Physiologyen_US
dc.subject.meshApoptosis Regulatory Proteins - Biosynthesis - Genetics - Metabolismen_US
dc.subject.meshBase Sequence - Geneticsen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshCerebellum - Cytology - Metabolismen_US
dc.subject.meshCytoplasmic Granules - Genetics - Metabolismen_US
dc.subject.meshFas Ligand Protein - Genetics - Metabolismen_US
dc.subject.meshGenes, Dominant - Physiologyen_US
dc.subject.meshGenes, Jun - Physiologyen_US
dc.subject.meshMembrane Proteins - Genetics - Metabolismen_US
dc.subject.meshNeurons - Cytology - Metabolismen_US
dc.subject.meshNeuropeptides - Biosynthesis - Geneticsen_US
dc.subject.meshPotassium - Metabolismen_US
dc.subject.meshProto-Oncogene Proteins - Genetics - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshResponse Elements - Physiologyen_US
dc.subject.meshSequence Deletionen_US
dc.subject.meshTranscription, Genetic - Physiologyen_US
dc.subject.meshUp-Regulation - Physiologyen_US
dc.titledp5/HRK is a c-jun target gene and required for apoptosis induced by potassium deprivation in cerebellar granule neuronsen_US
dc.typeArticleen_US
dc.identifier.emailChing, YP:ypching@hku.hken_US
dc.identifier.authorityChing, YP=rp00469en_US
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1074/jbc.M608694200en_US
dc.identifier.pmid17428807-
dc.identifier.scopuseid_2-s2.0-35648958679en_US
dc.identifier.hkuros143722-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-35648958679&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume282en_US
dc.identifier.issue42en_US
dc.identifier.spage30901en_US
dc.identifier.epage30909en_US
dc.identifier.isiWOS:000250136300058-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridMa, C=35080792100en_US
dc.identifier.scopusauthoridYing, C=21740028600en_US
dc.identifier.scopusauthoridYuan, Z=7401476600en_US
dc.identifier.scopusauthoridSong, B=35234938900en_US
dc.identifier.scopusauthoridLi, D=26324923700en_US
dc.identifier.scopusauthoridLiu, Y=35488192700en_US
dc.identifier.scopusauthoridLai, B=22951366000en_US
dc.identifier.scopusauthoridLi, W=8853055600en_US
dc.identifier.scopusauthoridChen, R=7406315258en_US
dc.identifier.scopusauthoridChing, YP=7005431277en_US
dc.identifier.scopusauthoridLi, M=12765700400en_US

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