File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: E2F1 is not essential for apoptosis induced by potassium deprivation in cerebellar granule neurons

TitleE2F1 is not essential for apoptosis induced by potassium deprivation in cerebellar granule neurons
Authors
Issue Date2007
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neulet
Citation
Neuroscience Letters, 2007, v. 424 n. 3, p. 155-159 How to Cite?
AbstractCerebellar granule neurons (CGNs) undergo apoptosis when deprived of depolarizing concentration of potassium. A key regulator of cell cycle, E2F1, was believed to play a role in CGN apoptosis induced by potassium deprivation. However, here we demonstrated that although E2F1 was upregulated in wild type CGNs following potassium deprivation, CGNs that derived from E2F1 knockout mice underwent apoptosis at a similar rate as the wild type. Analysis of the apoptotic neurons revealed no difference in the activation of caspase-3 in E2F1 null and wild type CGNs. Furthermore, knockdown of E2F1 expression by RNA interference failed to attenuate the apoptosis of CGNs induced by potassium deprivation. Taken together, our results suggested that E2F1 is not essential for apoptosis induced by potassium deprivation in CGNs. © 2007 Elsevier Ireland Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/58224
ISSN
2015 Impact Factor: 2.107
2015 SCImago Journal Rankings: 1.035
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYuan, Zen_HK
dc.contributor.authorMei, Yen_HK
dc.contributor.authorZhou, Jen_HK
dc.contributor.authorTan, Men_HK
dc.contributor.authorSong, Ben_HK
dc.contributor.authorMa, Cen_HK
dc.contributor.authorYing, Cen_HK
dc.contributor.authorLi, Den_HK
dc.contributor.authorChing, YPen_HK
dc.contributor.authorLi, Men_HK
dc.date.accessioned2010-05-31T03:26:08Z-
dc.date.available2010-05-31T03:26:08Z-
dc.date.issued2007en_HK
dc.identifier.citationNeuroscience Letters, 2007, v. 424 n. 3, p. 155-159en_HK
dc.identifier.issn0304-3940en_HK
dc.identifier.urihttp://hdl.handle.net/10722/58224-
dc.description.abstractCerebellar granule neurons (CGNs) undergo apoptosis when deprived of depolarizing concentration of potassium. A key regulator of cell cycle, E2F1, was believed to play a role in CGN apoptosis induced by potassium deprivation. However, here we demonstrated that although E2F1 was upregulated in wild type CGNs following potassium deprivation, CGNs that derived from E2F1 knockout mice underwent apoptosis at a similar rate as the wild type. Analysis of the apoptotic neurons revealed no difference in the activation of caspase-3 in E2F1 null and wild type CGNs. Furthermore, knockdown of E2F1 expression by RNA interference failed to attenuate the apoptosis of CGNs induced by potassium deprivation. Taken together, our results suggested that E2F1 is not essential for apoptosis induced by potassium deprivation in CGNs. © 2007 Elsevier Ireland Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neuleten_HK
dc.relation.ispartofNeuroscience Lettersen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAnimals, Newbornen_HK
dc.subject.meshApoptosis - drug effects - genetics - physiologyen_HK
dc.subject.meshCell Count - methodsen_HK
dc.subject.meshCells, Cultureden_HK
dc.subject.meshCerebellum - cytologyen_HK
dc.subject.meshDose-Response Relationship, Drugen_HK
dc.subject.meshE2F1 Transcription Factor - deficiency - physiologyen_HK
dc.subject.meshGene Expression Regulation - drug effects - physiologyen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Knockouten_HK
dc.subject.meshNeurons - drug effects - physiologyen_HK
dc.subject.meshPotassium - pharmacologyen_HK
dc.subject.meshRNA Interference - physiologyen_HK
dc.subject.meshTime Factorsen_HK
dc.titleE2F1 is not essential for apoptosis induced by potassium deprivation in cerebellar granule neuronsen_HK
dc.typeArticleen_HK
dc.identifier.emailChing, YP:ypching@hku.hken_HK
dc.identifier.authorityChing, YP=rp00469en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.neulet.2007.07.031en_HK
dc.identifier.pmid17728064-
dc.identifier.scopuseid_2-s2.0-34548621284en_HK
dc.identifier.hkuros143729en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34548621284&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume424en_HK
dc.identifier.issue3en_HK
dc.identifier.spage155en_HK
dc.identifier.epage159en_HK
dc.identifier.isiWOS:000250192500003-
dc.publisher.placeIrelanden_HK
dc.identifier.scopusauthoridYuan, Z=7401476600en_HK
dc.identifier.scopusauthoridMei, Y=7102674721en_HK
dc.identifier.scopusauthoridZhou, J=7405545445en_HK
dc.identifier.scopusauthoridTan, M=21740168400en_HK
dc.identifier.scopusauthoridSong, B=35234938900en_HK
dc.identifier.scopusauthoridMa, C=35080792100en_HK
dc.identifier.scopusauthoridYing, C=21740028600en_HK
dc.identifier.scopusauthoridLi, D=26324923700en_HK
dc.identifier.scopusauthoridChing, YP=7005431277en_HK
dc.identifier.scopusauthoridLi, M=12765700400en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats