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Conference Paper: The role of Pax6 in Beta-Amyloid toxicity and Alzheimer’s disease

TitleThe role of Pax6 in Beta-Amyloid toxicity and Alzheimer’s disease
Authors
Issue Date2011
PublisherThe University of Hong Kong.
Citation
Hong Kong Inter-University Biochemistry Postgraduate Symposium, The University of Hong Kong, Hong Kong, 11 June 2011, Poster Presentation: P-H028 How to Cite?
Abstract
Alzheimer’s disease (AD) is a progressive neurological disorder which is characterized by the neuronal dysfunction and loss in the patient brain. Previous studies has shown that cell cycle components such as Cyclin dependent kinase 4(CDK4), pRb and transcription factor E2F1/DP-1/C-Myb play critical roles in various models of AD. However, the mechanism by which cell cycle proteins regulate neuronal loss, especially the downstream events of this pathway are largely unknown. In this study, we identified a novel E2F1/C-Myb target gene Pax6, a key transcription factor essential for the development of brain, eye and pancreas, as an important regulator of neuronal cell death evoked by Beta-Amyloid(1-42)( A􀈕1-42) treatment.We found that siRNA-mediated knockdown of Pax6 protects cultured mouse cortical neurons from A􀈕1-42 induced neuronal death. Also we found that Pax6 mRNA/protein levels and transcriptional activity increase with A􀈕1-42 treatment in neurons and in APP mutant cell lines.We also showed that the endogenous induction of Pax6 by A􀈕1-42 treatment can be significantly blocked by the CDK4 inhibitors and Pax6 might be a target gene of CDK4/E2F1/C-Myb related cell cycle apoptosis pathway in this death model. Moreover, Pax6 is elevated in cortical neurons of entorhinal cortex, a brain region affected by AD, in an APP transgenic mouse model. Taken together, Pax6 is required for A􀈕1-42 induced neuronal apoptosis and play an important role in Alzheimer’s disease pathogenesis. This study may provide insights into development of therapeutic agents and approaches for AD through inhibition of Pax6 which has lower expression in normal adult brain.
Persistent Identifierhttp://hdl.handle.net/10722/140074

 

DC FieldValueLanguage
dc.contributor.authorZhang, Yen_US
dc.contributor.authorZhang, Yen_US
dc.contributor.authorJin, Den_US
dc.contributor.authorSong, Yen_US
dc.date.accessioned2011-09-23T06:06:19Z-
dc.date.available2011-09-23T06:06:19Z-
dc.date.issued2011en_US
dc.identifier.citationHong Kong Inter-University Biochemistry Postgraduate Symposium, The University of Hong Kong, Hong Kong, 11 June 2011, Poster Presentation: P-H028en_US
dc.identifier.urihttp://hdl.handle.net/10722/140074-
dc.description.abstractAlzheimer’s disease (AD) is a progressive neurological disorder which is characterized by the neuronal dysfunction and loss in the patient brain. Previous studies has shown that cell cycle components such as Cyclin dependent kinase 4(CDK4), pRb and transcription factor E2F1/DP-1/C-Myb play critical roles in various models of AD. However, the mechanism by which cell cycle proteins regulate neuronal loss, especially the downstream events of this pathway are largely unknown. In this study, we identified a novel E2F1/C-Myb target gene Pax6, a key transcription factor essential for the development of brain, eye and pancreas, as an important regulator of neuronal cell death evoked by Beta-Amyloid(1-42)( A􀈕1-42) treatment.We found that siRNA-mediated knockdown of Pax6 protects cultured mouse cortical neurons from A􀈕1-42 induced neuronal death. Also we found that Pax6 mRNA/protein levels and transcriptional activity increase with A􀈕1-42 treatment in neurons and in APP mutant cell lines.We also showed that the endogenous induction of Pax6 by A􀈕1-42 treatment can be significantly blocked by the CDK4 inhibitors and Pax6 might be a target gene of CDK4/E2F1/C-Myb related cell cycle apoptosis pathway in this death model. Moreover, Pax6 is elevated in cortical neurons of entorhinal cortex, a brain region affected by AD, in an APP transgenic mouse model. Taken together, Pax6 is required for A􀈕1-42 induced neuronal apoptosis and play an important role in Alzheimer’s disease pathogenesis. This study may provide insights into development of therapeutic agents and approaches for AD through inhibition of Pax6 which has lower expression in normal adult brain.-
dc.languageengen_US
dc.publisherThe University of Hong Kong.-
dc.relation.ispartofHong Kong Inter-University Biochemistry Postgraduate Symposiumen_US
dc.titleThe role of Pax6 in Beta-Amyloid toxicity and Alzheimer’s diseaseen_US
dc.typeConference_Paperen_US
dc.identifier.emailJin, D: dyjin@hku.hken_US
dc.identifier.emailSong, Y: songy@hku.hken_US
dc.identifier.authorityJin, D=rp00452en_US
dc.identifier.authoritySong, Y=rp00488en_US
dc.identifier.hkuros192389en_US
dc.publisher.placeHong Kong, China-

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