Zinc enhances synthesis of presenilin 1 in mouse primary cortical culture

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dc.contributor.authorPark, IHko
dc.contributor.authorJung, MWko
dc.contributor.authorMori, Hko
dc.contributor.authorMook-Jung, Iko
dc.date.accessioned2013-03-06T05:46:43Z-
dc.date.available2013-03-06T05:46:43Z-
dc.date.created2013-02-20-
dc.date.created2013-02-20-
dc.date.issued2001-07-
dc.identifier.citationBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.285, no.3, pp.680 - 688-
dc.identifier.issn0006-291X-
dc.identifier.urihttp://hdl.handle.net/10203/86004-
dc.description.abstractWhether zinc interacts with presenilin 1 (PS1), one of the causative genes of familial Alzheimer's disease (AD), is not known. Here we report that zinc modulates the synthesis of PSI. Exogenous zinc enhanced the amount of C-terminal fragments of PS1 (PS1-CTF) in neonatal mouse cortical cultures in a dose-dependent manner. Zinc also induced cell death in a dose-dependent manner. These effects of zinc were not mimicked by calcium, copper, or iron, and were blocked by a zinc-specific chelator, TPEN. Experiments using metabolic labeling and cycloheximide treatment revealed that zinc increased PS1-CTF by elevating the de novo synthesis of PS1. Time course experiments revealed that cell death commenced sooner (0.5-1 h) than enhancement of PS1-CTF (1-2 h) following zinc treatment. However, the amount of PS1-CTF remained unchanged during etoposide- or H2O2-induced cell death, suggesting that enhancement of PSI synthesis is specifically correlated with zinc-induced cell death. (C) 2001 Academic Press.-
dc.languageEnglish-
dc.publisherACADEMIC PRESS INC-
dc.subjectAMYLOID PRECURSOR PROTEIN-
dc.subjectGAMMA-SECRETASE ACTIVITY-
dc.subjectHISTOCHEMICALLY-REACTIVE ZINC-
dc.subjectALZHEIMER A-BETA-
dc.subjectTRANSGENIC MICE-
dc.subjectDISEASE-
dc.subjectNEURONS-
dc.subjectBRAIN-
dc.subjectENDOPROTEOLYSIS-
dc.subjectAPOPTOSIS-
dc.titleZinc enhances synthesis of presenilin 1 in mouse primary cortical culture-
dc.typeArticle-
dc.identifier.wosid000170131400018-
dc.identifier.scopusid2-s2.0-0034811346-
dc.type.rimsART-
dc.citation.volume285-
dc.citation.issue3-
dc.citation.beginningpage680-
dc.citation.endingpage688-
dc.citation.publicationnameBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS-
dc.identifier.doi10.1006/bbrc.2001.5243-
dc.contributor.localauthorJung, MW-
dc.contributor.nonIdAuthorPark, IH-
dc.contributor.nonIdAuthorMori, H-
dc.contributor.nonIdAuthorMook-Jung, I-
dc.type.journalArticleArticle-
dc.subject.keywordAuthorAlzheimer&apos-
dc.subject.keywordAuthors disease-
dc.subject.keywordAuthorpresenilin 1-
dc.subject.keywordAuthorzinc-
dc.subject.keywordAuthorbeta amyloid-
dc.subject.keywordAuthorcell death-
dc.subject.keywordAuthorTPEN-
dc.subject.keywordPlusAMYLOID PRECURSOR PROTEIN-
dc.subject.keywordPlusGAMMA-SECRETASE ACTIVITY-
dc.subject.keywordPlusHISTOCHEMICALLY-REACTIVE ZINC-
dc.subject.keywordPlusALZHEIMER A-BETA-
dc.subject.keywordPlusTRANSGENIC MICE-
dc.subject.keywordPlusDISEASE-
dc.subject.keywordPlusNEURONS-
dc.subject.keywordPlusBRAIN-
dc.subject.keywordPlusENDOPROTEOLYSIS-
dc.subject.keywordPlusAPOPTOSIS-
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