Negative regulation of the SAPK/JNK signaling pathway by presenilin 1

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dc.contributor.authorKim, Jin Wooko
dc.contributor.authorChang, Tong-Shinko
dc.contributor.authorLee, Ji Eunko
dc.contributor.authorHuh, Sung-Hoko
dc.contributor.authorYeon, Seung Wooko
dc.contributor.authorYang, Wan Seokko
dc.contributor.authorJoe, Cheol O.ko
dc.contributor.authorMook-Jung, Inheeko
dc.contributor.authorTanzi, Rudolph E.ko
dc.contributor.authorKim, Tae-Wanko
dc.contributor.authorJoe, Cheol Oko
dc.date.accessioned2010-04-05T02:15:00Z-
dc.date.available2010-04-05T02:15:00Z-
dc.date.created2012-02-06-
dc.date.created2012-02-06-
dc.date.issued2001-04-
dc.identifier.citationJOURNAL OF CELL BIOLOGY, v.153, no.3, pp.457 - 463-
dc.identifier.issn0021-9525-
dc.identifier.urihttp://hdl.handle.net/10203/17520-
dc.description.abstractPresenilin 1 (PS1) plays a pivotal role in Notch signaling and the intracellular metabolism of the amyloid beta -protein, To understand intracellular signaling events downstream of PSI, we investigated in this study the action of PS1 on mitogen-activated protein kinase pathways. Overexpressed PS1 suppressed the stress-induced stimulation of stress-activated protein kinase (SAPK)/c-Jun NH2-terminal kinase (JNK) in human embryonic kidney 293 cells. Interestingly, two functionally inactive PSI mutants, PS1(D257A) and PS1(D385A), failed to inhibit UV-stimulated SAPK/ JNK. Furthermore, H2O2- or UV-stimulated SAPK activity was higher in mouse embryonic fibroblast (MEF) cells from PS1-null mice than in MEF cells from PS+/+ mice. MEFPS1(-/-) cells were more sensitive to the H2O2-induced apoptosis than MEFPS1(+/+) cells. Ectopic expression of PS1 in MEFPS1(-/-) cells suppressed H2O2-stimulated SAPK/JNK activity and apoptotic cell death. Together, our data suggest that PS1 inhibits the stress-activated signaling by suppressing the SAPK/ JNK pathway.-
dc.description.sponsorshipa National Creative Research Initiative Center for Cell Death, Graduate School of Biotechnology, Korea University, Seoul, 136-701, Korea b Brain Disease Research Center, Ajou University School of Medicine, Suwon, Kyongki-do, Korea c Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Taejon, 305-701, Korea d Genetics and Aging Research Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129en
dc.languageEnglish-
dc.language.isoen_USen
dc.publisherROCKEFELLER UNIV PRESS-
dc.subjectFAMILIAL ALZHEIMERS-DISEASE-
dc.subjectAMYLOID PRECURSOR PROTEIN-
dc.subjectMAP KINASES-
dc.subjectMISSENSE MUTATIONS-
dc.subjectINDUCED APOPTOSIS-
dc.subjectMAMMALIAN-CELLS-
dc.subjectGENE-
dc.subjectNOTCH-
dc.subjectJNK-
dc.subjectSTRESS-
dc.titleNegative regulation of the SAPK/JNK signaling pathway by presenilin 1-
dc.typeArticle-
dc.identifier.wosid000168481400003-
dc.identifier.scopusid2-s2.0-0035809240-
dc.type.rimsART-
dc.citation.volume153-
dc.citation.issue3-
dc.citation.beginningpage457-
dc.citation.endingpage463-
dc.citation.publicationnameJOURNAL OF CELL BIOLOGY-
dc.identifier.doi10.1083/jcb.153.3.457-
dc.embargo.liftdate9999-12-31-
dc.embargo.terms9999-12-31-
dc.contributor.localauthorKim, Jin Woo-
dc.contributor.localauthorJoe, Cheol O-
dc.contributor.nonIdAuthorChang, Tong-Shin-
dc.contributor.nonIdAuthorLee, Ji Eun-
dc.contributor.nonIdAuthorHuh, Sung-Ho-
dc.contributor.nonIdAuthorYeon, Seung Woo-
dc.contributor.nonIdAuthorYang, Wan Seok-
dc.contributor.nonIdAuthorJoe, Cheol O.-
dc.contributor.nonIdAuthorMook-Jung, Inhee-
dc.contributor.nonIdAuthorTanzi, Rudolph E.-
dc.contributor.nonIdAuthorKim, Tae-Wan-
dc.type.journalArticleArticle-
dc.subject.keywordAuthorapoptosis-
dc.subject.keywordAuthorc-Jun NH2-terminal kinase-
dc.subject.keywordAuthorpresenilin 1-
dc.subject.keywordAuthorgamma-secretase-
dc.subject.keywordAuthorstress-activated protein kinase-
dc.subject.keywordPlusFAMILIAL ALZHEIMERS-DISEASE-
dc.subject.keywordPlusAMYLOID PRECURSOR PROTEIN-
dc.subject.keywordPlusMAP KINASES-
dc.subject.keywordPlusMISSENSE MUTATIONS-
dc.subject.keywordPlusINDUCED APOPTOSIS-
dc.subject.keywordPlusMAMMALIAN-CELLS-
dc.subject.keywordPlusGENE-
dc.subject.keywordPlusNOTCH-
dc.subject.keywordPlusJNK-
dc.subject.keywordPlusSTRESS-
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