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Article: Enhanced ROS generation mediated by alzheimer's disease presenilin regulation of InsP 3R Ca 2+ signaling

TitleEnhanced ROS generation mediated by alzheimer's disease presenilin regulation of InsP 3R Ca 2+ signaling
Authors
Issue Date2011
PublisherMary Ann Liebert, Inc Publishers. The Journal's web site is located at http://www.liebertpub.com/ars
Citation
Antioxidants And Redox Signaling, 2011, v. 14 n. 7, p. 1225-1235 How to Cite?
AbstractFamilial Alzheimer's disease (FAD) is caused by mutations in amyloid precursor protein and presenilins (PS1, PS2). Many FAD-linked PS mutations affect intracellular calcium (Ca 2+) homeostasis by proximal mechanisms independent of amyloid production by dramatically enhancing gating of the inositol trisphosphate receptor (InsP 3R) intracellular Ca 2+ release channel by a gain-of-function effect that mirrors genetics of FAD and is independent of secretase activity. Electrophysiological recordings of InsP 3R in FAD patient B cells, cortical neurons of asymptomatic PS1-AD mice, and other cells revealed they have higher occupancy in a high open probability burst mode, resulting in enhanced Ca 2+ signaling. Exaggerated Ca 2+ signaling through this mechanism results in enhanced generation of reactive oxygen species, believed to be an important component in AD pathogenesis. Exaggerated Ca 2+ signaling through InsP 3R-PS interaction is a disease specific and robust proximal mechanism in AD that may contribute to the pathology of AD by enhanced generation of reactive oxygen species. © 2011 Mary Ann Liebert, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/132531
ISSN
2015 Impact Factor: 7.093
2015 SCImago Journal Rankings: 3.134
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
American Health Assistance FoundationA2008-137
NIHGM56328
MH059937
Alzheimer's Disease Core Center at the University of PennsylvaniaAG 10124
Funding Information:

Acknowledgement is made to the donors of Alzheimer's Disease Research, a program of the American Health Assistance Foundation (A2008-137 to J.K.F.), NIH GM56328 and MH059937 to JKF and the Alzheimer's Disease Core Center at the University of Pennsylvania (AG 10124).

References

 

DC FieldValueLanguage
dc.contributor.authorMüller, Men_HK
dc.contributor.authorCheung, KHen_HK
dc.contributor.authorFoskett, JKen_HK
dc.date.accessioned2011-03-28T09:26:00Z-
dc.date.available2011-03-28T09:26:00Z-
dc.date.issued2011en_HK
dc.identifier.citationAntioxidants And Redox Signaling, 2011, v. 14 n. 7, p. 1225-1235en_HK
dc.identifier.issn1523-0864en_HK
dc.identifier.urihttp://hdl.handle.net/10722/132531-
dc.description.abstractFamilial Alzheimer's disease (FAD) is caused by mutations in amyloid precursor protein and presenilins (PS1, PS2). Many FAD-linked PS mutations affect intracellular calcium (Ca 2+) homeostasis by proximal mechanisms independent of amyloid production by dramatically enhancing gating of the inositol trisphosphate receptor (InsP 3R) intracellular Ca 2+ release channel by a gain-of-function effect that mirrors genetics of FAD and is independent of secretase activity. Electrophysiological recordings of InsP 3R in FAD patient B cells, cortical neurons of asymptomatic PS1-AD mice, and other cells revealed they have higher occupancy in a high open probability burst mode, resulting in enhanced Ca 2+ signaling. Exaggerated Ca 2+ signaling through this mechanism results in enhanced generation of reactive oxygen species, believed to be an important component in AD pathogenesis. Exaggerated Ca 2+ signaling through InsP 3R-PS interaction is a disease specific and robust proximal mechanism in AD that may contribute to the pathology of AD by enhanced generation of reactive oxygen species. © 2011 Mary Ann Liebert, Inc.en_HK
dc.languageengen_US
dc.publisherMary Ann Liebert, Inc Publishers. The Journal's web site is located at http://www.liebertpub.com/arsen_HK
dc.relation.ispartofAntioxidants and Redox Signalingen_HK
dc.titleEnhanced ROS generation mediated by alzheimer's disease presenilin regulation of InsP 3R Ca 2+ signalingen_HK
dc.typeArticleen_HK
dc.identifier.emailCheung, KH: kingho.cheung@hku.hken_HK
dc.identifier.authorityCheung, KH=rp01463en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1089/ars.2010.3421en_HK
dc.identifier.pmid20701429-
dc.identifier.pmcidPMC3048838-
dc.identifier.scopuseid_2-s2.0-78650436415en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-78650436415&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume14en_HK
dc.identifier.issue7en_HK
dc.identifier.spage1225en_HK
dc.identifier.epage1235en_HK
dc.identifier.isiWOS:000288157300005-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridMüller, M=7404689330en_HK
dc.identifier.scopusauthoridCheung, KH=14007487800en_HK
dc.identifier.scopusauthoridFoskett, JK=7005723620en_HK
dc.identifier.citeulike10856168-

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