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The protein p17 signaling pathways in cancer

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dc.contributor.authorHeese, Klaus-
dc.date.accessioned2022-07-16T07:03:15Z-
dc.date.available2022-07-16T07:03:15Z-
dc.date.created2021-05-12-
dc.date.issued2013-12-
dc.identifier.issn1010-4283-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/161268-
dc.description.abstractP17 is a novel neuronal protein expressed under physiological conditions only at very low levels in other tissues. Accumulating data indicate its crucial involvement in tumorigenic effects. Using molecular, cellular, and biocomputational methods, the current study unraveled p17 mode of action. Data indicate that mitochondria-associated p17 interacts with the proteins TMEM115, YPEL3, ERP44, CDK5RAP, and NNAT. Moreover, p17 drives the cell cycle into the G0/G1 phase and enhances survival of proliferating cells. Interference with p17 activities thus might become a novel option to influence also the tumor suppressor protein p53 signaling pathways for the treatment of tumors.-
dc.language영어-
dc.language.isoen-
dc.publisherSAGE PUBLICATIONS LTD-
dc.titleThe protein p17 signaling pathways in cancer-
dc.typeArticle-
dc.contributor.affiliatedAuthorHeese, Klaus-
dc.identifier.doi10.1007/s13277-013-0999-1-
dc.identifier.scopusid2-s2.0-84891491280-
dc.identifier.wosid000328292100098-
dc.identifier.bibliographicCitationTUMOR BIOLOGY, v.34, no.6, pp.4081 - 4087-
dc.relation.isPartOfTUMOR BIOLOGY-
dc.citation.titleTUMOR BIOLOGY-
dc.citation.volume34-
dc.citation.number6-
dc.citation.startPage4081-
dc.citation.endPage4087-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaOncology-
dc.relation.journalWebOfScienceCategoryOncology-
dc.subject.keywordPlusURACIL-DNA GLYCOSYLASE-
dc.subject.keywordPlusBASE EXCISION-REPAIR-
dc.subject.keywordPlusWIP1 PHOSPHATASE-
dc.subject.keywordPlusP53-
dc.subject.keywordPlusGENE-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusYPEL3-
dc.subject.keywordPlusMECHANISMS-
dc.subject.keywordPlusINSIGHTS-
dc.subject.keywordPlusUGENE-
dc.subject.keywordAuthorCancer-
dc.subject.keywordAuthorOncology-
dc.subject.keywordAuthorFAM72A-
dc.subject.keywordAuthorUgene-
dc.subject.keywordAuthorp53-
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서울 의생명공학전문대학원 > 서울 의생명공학전문대학원 > 1. Journal Articles

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Heese, Klaus
GRADUATE SCHOOL OF BIOMEDICAL SCIENCE AND ENGINEERING (DEPARTMENT OF BIOMEDICAL SCIENCE)
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