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ER Stress Induces the Expression of Jpk, which Inhibits Cell Cycle Progression in F9 Teratocarcinoma Cell

DC Field Value Language
dc.contributor.author공경아-
dc.contributor.author김명희-
dc.contributor.author정현주-
dc.date.accessioned2014-12-21T16:24:11Z-
dc.date.available2014-12-21T16:24:11Z-
dc.date.issued2007-
dc.identifier.issn0077-8923-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/95626-
dc.description.abstractJopock (Jpk), a transacting factor associated with the position-specific regulatory element of murine Hoxa-7, has shown to induce cell death in both prokaryotic and eukaryotic cells when introduced and overexpressed. Since Jpk protein harbors a transmembrane domain (TM) and a putative endoplasmic reticulum (ER) -retention signal at the N terminus, a subcellular localization of the protein was analyzed after fusing it into the green fluorescent protein (GFP). Both N–term- (Jpk-EGFP) and C–term-fused Jpk (EGFP-Jpk) showed to be localized in the ER when analyzed under the fluorescence microscope after staining the cells with ER- and Mito-Tracker. Through deletion analysis TM turned out to be important for ER localization of Jpk. When flow cytometric analysis was performed, both cells expressing Jpk-EGFP and EGFP-Jpk led cell cycle arrest and subsequent apoptotic cell death. In order to see whether Jpk is expressed during ER stress-mediated apoptosis, F9 cells were treated with DTT, an ER stress inducer. In the presence of 4 mM of DTT, about 50% of cells died strongly expressing Jpk (sevenfold) as well as Grp78, a molecular chaperone, and CHOP-10, a well-known apoptotic protein. When cells were transfected with both pEGFP-Jpk and pJpk-EGFP, cell cycle progression was interrupted compared to those of control cells. In summary, excess ER stress upregulated the expression of Jpk, which seemed to inhibit the cell cycle progression. These results altogether suggest that Jpk could be a useful cell death-triggering molecule applicable for cancer therapy as well as a useful target molecule for the treatment of certain neurodegenerative diseases caused by ER stress.-
dc.description.statementOfResponsibilityopen-
dc.format.extent76~81-
dc.relation.isPartOfANNALS OF THE NEW YORK ACADEMY OF SCIENCES-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleER Stress Induces the Expression of Jpk, which Inhibits Cell Cycle Progression in F9 Teratocarcinoma Cell-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Anatomy (해부학)-
dc.contributor.googleauthorHYE SUN KIM-
dc.contributor.googleauthorKYOUNG-AH KONG-
dc.contributor.googleauthorMYOUNG HEE KIM-
dc.contributor.googleauthorSUNGDO PARK-
dc.contributor.googleauthorHYUNJOO CHUNG-
dc.identifier.doi10.1196/annals.1397.011-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00158-
dc.contributor.localIdA00432-
dc.contributor.localIdA03769-
dc.relation.journalcodeJ00181-
dc.identifier.eissn1749-6632-
dc.identifier.urlhttp://onlinelibrary.wiley.com/doi/10.1196/annals.1397.011/abstract-
dc.contributor.alternativeNameKong, Kyoung Ah-
dc.contributor.alternativeNameKim, Myoung Hee-
dc.contributor.alternativeNameChung, Huyun Joo-
dc.contributor.affiliatedAuthorKong, Kyoung Ah-
dc.contributor.affiliatedAuthorKim, Myoung Hee-
dc.contributor.affiliatedAuthorChung, Huyun Joo-
dc.rights.accessRightsnot free-
dc.citation.volume1095-
dc.citation.startPage76-
dc.citation.endPage81-
dc.identifier.bibliographicCitationANNALS OF THE NEW YORK ACADEMY OF SCIENCES, Vol.1095 : 76-81, 2007-
dc.identifier.rimsid44975-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Anatomy (해부학교실) > 1. Journal Papers

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