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Characterization of the novel protein P9TLDR (temporal lobe down-regulated) with a brain-site-specific gene expression modality in Alzheimer's disease brain

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dc.contributor.authorYokota, Tomoko-
dc.contributor.authorAkatsu, Hiroyasu-
dc.contributor.authorMiyauchi, Takashi-
dc.contributor.authorHeese, Klaus-
dc.date.accessioned2022-07-16T12:39:54Z-
dc.date.available2022-07-16T12:39:54Z-
dc.date.created2021-05-12-
dc.date.issued2012-12-
dc.identifier.issn0014-5793-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/164087-
dc.description.abstractAlzheimer's disease (AD) is an aging-related neurodegenerative disorder characterized by irreversible loss of higher cognitive functions. The disease is characterized by the presence of amyloid plaques and neurofibrillary tangles (NFT). In the current study we isolated from an intra-cerebral brain-site-specific (AD temporal lobe vs. AD occipital lobe) polymerase chain reaction (PCR)-select cDNA suppression subtractive hybridization (PCR-cDNA-SSH) expression analysis the novel gene P9TLDR, potentially a microtubule-associated protein involved in neuronal migration, with an altered expression pattern: down-regulated in the temporal lobe cortex of early stage AD brains. In an in vitro AD-related cell model, amyloid-beta peptide (A beta)-treated neurons, reduced P9TLDR expression correlated with increased tau protein phosphorylation. In conclusion, interference with the P9TLDR signalling pathways might be a therapeutic strategy for the treatment of AD.-
dc.language영어-
dc.language.isoen-
dc.publisherElsevier B.V.-
dc.titleCharacterization of the novel protein P9TLDR (temporal lobe down-regulated) with a brain-site-specific gene expression modality in Alzheimer's disease brain-
dc.typeArticle-
dc.contributor.affiliatedAuthorHeese, Klaus-
dc.identifier.doi10.1016/j.febslet.2012.10.050-
dc.identifier.scopusid2-s2.0-84870565960-
dc.identifier.wosid000312004400017-
dc.identifier.bibliographicCitationFEBS LETTERS, v.586, no.24, pp.4357 - 4361-
dc.relation.isPartOfFEBS LETTERS-
dc.citation.titleFEBS LETTERS-
dc.citation.volume586-
dc.citation.number24-
dc.citation.startPage4357-
dc.citation.endPage4361-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-
dc.relation.journalResearchAreaBiophysics-
dc.relation.journalResearchAreaCell Biology-
dc.relation.journalWebOfScienceCategoryBiochemistry & Molecular Biology-
dc.relation.journalWebOfScienceCategoryBiophysics-
dc.relation.journalWebOfScienceCategoryCell Biology-
dc.subject.keywordPlusSUPPRESSION SUBTRACTIVE HYBRIDIZATION-
dc.subject.keywordAuthorAlzheimer&apos-
dc.subject.keywordAuthors disease-
dc.subject.keywordAuthorAmyloid-
dc.subject.keywordAuthorBrain-
dc.subject.keywordAuthorMapt-
dc.subject.keywordAuthorNeurotoxicity-
dc.subject.keywordAuthorNeurodegeneration-
dc.subject.keywordAuthorTau-
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서울 의생명공학전문대학원 > 서울 의생명공학전문대학원 > 1. Journal Articles

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GRADUATE SCHOOL OF BIOMEDICAL SCIENCE AND ENGINEERING (DEPARTMENT OF BIOMEDICAL SCIENCE)
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