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Article: The presenilin-2 loop peptide perturbs intracellular Ca2+ homeostasis and accelerates apoptosis

TitleThe presenilin-2 loop peptide perturbs intracellular Ca2+ homeostasis and accelerates apoptosis
Authors
KeywordsChemicals And Cas Registry Numbers
Issue Date2006
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, 2006, v. 281 n. 24, p. 16649-16655 How to Cite?
AbstractIn cells undergoing apoptosis, a 22-amino-acid presenilin-2-loop peptide (PS2-LP, amino acids 308-329 in presenilin-2) is generated through cleavage of the carboxyl-terminal fragment of presenilin-2 by caspase-3. The impact of PS2-LP on the progression of apoptosis, however, is not known. Here we show that PS2-LP is a potent inducer of the mitochondrial-dependent cell death pathway when transduced as a fusion protein with HIV-TAT. Biochemical and functional studies demonstrate that TAT-PS2-LP can interact with the inositol 1,4,5-trisphosphate receptor and activate Ca2+ release from the endoplasmic reticulum. These results indicate that PS2-LP-mediated alteration of intracellular Ca2+ homeostasis may be linked to the acceleration of apoptosis. Therefore, targeting the function of PS2-LP could provide a useful therapeutic tool for the treatment of cancer and degenerative diseases. © 2006 by The American Society for Biochemistry and Molecular Biology, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/132539
ISSN
2015 Impact Factor: 4.258
2015 SCImago Journal Rankings: 3.151
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCai, Cen_HK
dc.contributor.authorLin, Pen_HK
dc.contributor.authorCheung, KHen_HK
dc.contributor.authorLi, Nen_HK
dc.contributor.authorLevchook, Cen_HK
dc.contributor.authorPan, Zen_HK
dc.contributor.authorFerrante, Cen_HK
dc.contributor.authorBoulianne, GLen_HK
dc.contributor.authorFoskett, JKen_HK
dc.contributor.authorDanielpour, Den_HK
dc.contributor.authorMa, Jen_HK
dc.date.accessioned2011-03-28T09:26:06Z-
dc.date.available2011-03-28T09:26:06Z-
dc.date.issued2006en_HK
dc.identifier.citationJournal Of Biological Chemistry, 2006, v. 281 n. 24, p. 16649-16655en_HK
dc.identifier.issn0021-9258en_HK
dc.identifier.urihttp://hdl.handle.net/10722/132539-
dc.description.abstractIn cells undergoing apoptosis, a 22-amino-acid presenilin-2-loop peptide (PS2-LP, amino acids 308-329 in presenilin-2) is generated through cleavage of the carboxyl-terminal fragment of presenilin-2 by caspase-3. The impact of PS2-LP on the progression of apoptosis, however, is not known. Here we show that PS2-LP is a potent inducer of the mitochondrial-dependent cell death pathway when transduced as a fusion protein with HIV-TAT. Biochemical and functional studies demonstrate that TAT-PS2-LP can interact with the inositol 1,4,5-trisphosphate receptor and activate Ca2+ release from the endoplasmic reticulum. These results indicate that PS2-LP-mediated alteration of intracellular Ca2+ homeostasis may be linked to the acceleration of apoptosis. Therefore, targeting the function of PS2-LP could provide a useful therapeutic tool for the treatment of cancer and degenerative diseases. © 2006 by The American Society for Biochemistry and Molecular Biology, Inc.en_HK
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_HK
dc.relation.ispartofJournal of Biological Chemistryen_HK
dc.subjectChemicals And Cas Registry Numbersen_US
dc.titleThe presenilin-2 loop peptide perturbs intracellular Ca2+ homeostasis and accelerates apoptosisen_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.doi10.1074/jbc.M512026200en_HK
dc.identifier.pmid16603547-
dc.identifier.scopuseid_2-s2.0-33745197557en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33745197557&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume281en_HK
dc.identifier.issue24en_HK
dc.identifier.spage16649en_HK
dc.identifier.epage16655en_HK
dc.identifier.eissn1083-351X-
dc.identifier.isiWOS:000238165700058-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridCai, C=23972233400en_HK
dc.identifier.scopusauthoridLin, P=13907342900en_HK
dc.identifier.scopusauthoridCheung, KH=14007487800en_HK
dc.identifier.scopusauthoridLi, N=36065390000en_HK
dc.identifier.scopusauthoridLevchook, C=14017905500en_HK
dc.identifier.scopusauthoridPan, Z=7402644656en_HK
dc.identifier.scopusauthoridFerrante, C=14017866500en_HK
dc.identifier.scopusauthoridBoulianne, GL=7003977689en_HK
dc.identifier.scopusauthoridFoskett, JK=7005723620en_HK
dc.identifier.scopusauthoridDanielpour, D=7004705477en_HK
dc.identifier.scopusauthoridMa, J=7406201001en_HK

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