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Conference Paper: EPAC2-deficiency leads to more severe neurological deficit and larger infarct with higher glial reactivity after transient middle cerebral occlusion

TitleEPAC2-deficiency leads to more severe neurological deficit and larger infarct with higher glial reactivity after transient middle cerebral occlusion
Authors
Cheng, LYeung, PKKChung, SSMChung, SK
Issue Date2011
PublisherISCBFM.
Citation
The 25th International Symosium on Cerebral Blood Flow, Metabolism, and Function & 10th International Conference on Quantification of Brain Function with PET (BRAIN’11 & BRAINPET’11), Barcelona, Spain, 25-28 May 2011. How to Cite?
AbstractINTRODUCTION: Exchange proteins activated by cAMP (Epac1 and Epac2) belong to a family of cAMP-regulated guanine nucleotide exchange factors (cAMPGEFs) for the small GTPases, Rap1 and Rap2[1]. Epac1 was thought to be important in maintenance of tight and adhesion junctions between endothelial cells[2] , suggesting that Epac may play an important role in blood brain barrier (BBB) function. OBJECTIVE: Previously, it was shown that Epac2 mRNA is expressed in the brain[3]. Here, the protein expression of Epac2 was determined and compared to that of Epac1. In addition, the role of Epac2 was determined in the BBB and brain function after ischemia/reperfusion injury. METHOD: Six regions of brain from Epac2 wild type (Epac2+/+) mice was dissected, and proteins were extracted in order to determine the expression of Epac1 and Epac2 under normal and …
DescriptionAbstract no. 912
Persistent Identifierhttp://hdl.handle.net/10722/165044

 

DC FieldValueLanguage
dc.contributor.authorCheng, Len_US
dc.contributor.authorYeung, PKKen_US
dc.contributor.authorChung, SSMen_US
dc.contributor.authorChung, SKen_US
dc.date.accessioned2012-09-20T08:13:51Z-
dc.date.available2012-09-20T08:13:51Z-
dc.date.issued2011en_US
dc.identifier.citationThe 25th International Symosium on Cerebral Blood Flow, Metabolism, and Function & 10th International Conference on Quantification of Brain Function with PET (BRAIN’11 & BRAINPET’11), Barcelona, Spain, 25-28 May 2011.en_US
dc.identifier.urihttp://hdl.handle.net/10722/165044-
dc.descriptionAbstract no. 912-
dc.description.abstractINTRODUCTION: Exchange proteins activated by cAMP (Epac1 and Epac2) belong to a family of cAMP-regulated guanine nucleotide exchange factors (cAMPGEFs) for the small GTPases, Rap1 and Rap2[1]. Epac1 was thought to be important in maintenance of tight and adhesion junctions between endothelial cells[2] , suggesting that Epac may play an important role in blood brain barrier (BBB) function. OBJECTIVE: Previously, it was shown that Epac2 mRNA is expressed in the brain[3]. Here, the protein expression of Epac2 was determined and compared to that of Epac1. In addition, the role of Epac2 was determined in the BBB and brain function after ischemia/reperfusion injury. METHOD: Six regions of brain from Epac2 wild type (Epac2+/+) mice was dissected, and proteins were extracted in order to determine the expression of Epac1 and Epac2 under normal and …-
dc.languageengen_US
dc.publisherISCBFM.-
dc.relation.ispartofISCBFM 2011 Conference Abstractsen_US
dc.titleEPAC2-deficiency leads to more severe neurological deficit and larger infarct with higher glial reactivity after transient middle cerebral occlusionen_US
dc.typeConference_Paperen_US
dc.identifier.emailYeung, PKK: ykkp@hkucc.hku.hken_US
dc.identifier.emailChung, SSM: smchung@hkucc.hku.hken_US
dc.identifier.emailChung, SK: skchung@hkucc.hku.hken_US
dc.identifier.authorityChung, SSM=rp00376en_US
dc.identifier.authorityChung, SK=rp00381en_US
dc.description.naturepostprint-
dc.identifier.hkuros211463en_US
dc.description.otherThe 25th International Symosium on Cerebral Blood Flow, Metabolism, and Function & 10th International Conference on Quantification of Brain Function with PET (BRAIN’11 & BRAINPET’11 ), Barcelona, Spain, 25-28 May 2011.-

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