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dc.creatorBajić, Vladan
dc.creatorSu, Bo
dc.creatorLee, Hyoung-Gon
dc.creatorKudo, Wataru
dc.creatorSiedlak, Sandra L.
dc.creatorŽivković, Lada
dc.creatorSpremo-Potparević, Biljana
dc.creatorĐelić, Ninoslav
dc.creatorMilicević, Zorana
dc.creatorSingh, Avneet K.
dc.creatorFahmy, Lara M.
dc.creatorWang, Xinglong
dc.creatorSmith, Mark A.
dc.creatorZhu, Xiongwei
dc.date.accessioned2020-06-03T13:27:52Z
dc.date.available2020-06-03T13:27:52Z
dc.date.issued2011
dc.identifier.issn1425-8153
dc.identifier.urihttps://vet-erinar.vet.bg.ac.rs/handle/123456789/800
dc.description.abstractPost-mitotic neurons are typically terminally differentiated and in a quiescent status. However, in Alzheimer disease (AD), many neurons display ectopic re-expression of cell cycle-related proteins. Cyclin-dependent kinase 11 (CDK11) mRNA produces a 110-kDa protein (CDK11(p110)) throughout the cell cycle, a 58-kDa protein (CDK11(p58)) that is specifically translated from an internal ribosome entry site and expressed only in the G(2)/M phase of the cell cycle, and a 46-kDa protein (CDK11(p46)) that is considered to be apoptosis specific. CDK11 is required for sister chromatid cohesion and the completion of mitosis. In this study, we found that the expression patterns of CDK11 vary such that cytoplasmic CDK11 is increased in AD cellular processes, compared to a pronounced nuclear expression pattern in most controls. We also investigated the effect of amyloid precursor protein (APP) on CDK11 expression in vitro by using M17 cells overexpressing wild-type APP and APP Swedish mutant phenotype and found increased CDK11 expression compared to empty vector. In addition, amyloid-beta(25-35) resulted in increased CDK11 in M17 cells. These data suggest that CDK11 may play a vital role in cell cycle re-entry in AD neurons in an APP-dependent manner, thus presenting an intriguing novel function of the APP signaling pathway in AD.en
dc.publisherBMC, London
dc.relationinfo:eu-repo/grantAgreement/MESTD/Basic Research (BR or ON)/173034/RS//
dc.relationNational Institutes of HealthUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USA [AG028679, AG031364]
dc.rightsopenAccess
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.sourceCellular & Molecular Biology Letters
dc.subjectAlzheimer diseaseen
dc.subjectAPPen
dc.subjectCDK11en
dc.subjectM17 cellsen
dc.titleMislocalization of CDK11/PITSLRE, a regulator of the G2/M phase of the cell cycle, in Alzheimer diseaseen
dc.typearticle
dc.rights.licenseBY
dcterms.abstractЗху, Xионгwеи; Смитх, Марк A.; Сингх, Aвнеет К.; Wанг, Xинглонг; Сиедлак, Сандра Л.; Кудо, Wатару; Лее, Хyоунг-Гон; Фахмy, Лара М.; Спремо-Потпаревић, Биљана; Живковић, Лада; Бајић, Владан; Су, Бо; Милицевић, Зорана; Ђелић, Нинослав;
dc.citation.volume16
dc.citation.issue3
dc.citation.spage359
dc.citation.epage372
dc.citation.other16(3): 359-372
dc.citation.rankM23
dc.identifier.wos000293019200001
dc.identifier.doi10.2478/s11658-011-0011-2
dc.identifier.pmid21461981
dc.identifier.scopus2-s2.0-80052519333
dc.identifier.fulltexthttps://vet-erinar.vet.bg.ac.rs/bitstream/id/1334/799.pdf
dc.type.versionpublishedVersion


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