Mislocalization of CDK11/PITSLRE, a regulator of the G2/M phase of the cell cycle, in Alzheimer disease
2011
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Аутори
Bajić, VladanSu, Bo
Lee, Hyoung-Gon
Kudo, Wataru
Siedlak, Sandra L.
Živković, Lada
Spremo-Potparević, Biljana
Đelić, Ninoslav
Milicević, Zorana
Singh, Avneet K.
Fahmy, Lara M.
Wang, Xinglong
Smith, Mark A.
Zhu, Xiongwei
Чланак у часопису (Објављена верзија)
Метаподаци
Приказ свих података о документуАпстракт
Post-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 phenoty...pe 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.
Кључне речи:
Alzheimer disease / APP / CDK11 / M17 cellsИзвор:
Cellular & Molecular Biology Letters, 2011, 16, 3, 359-372Издавач:
- BMC, London
Финансирање / пројекти:
- Аберације ћелијског циклуса и утицај оксидативног стреса на неуродегенеративне процесе и малигну трансформацију ћелије (RS-MESTD-Basic Research (BR or ON)-173034)
- National Institutes of HealthUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USA [AG028679, AG031364]
DOI: 10.2478/s11658-011-0011-2
ISSN: 1425-8153
PubMed: 21461981
WoS: 000293019200001
Scopus: 2-s2.0-80052519333
Колекције
Институција/група
Fakultet veterinarske medicineTY - JOUR AU - Bajić, Vladan AU - Su, Bo AU - Lee, Hyoung-Gon AU - Kudo, Wataru AU - Siedlak, Sandra L. AU - Živković, Lada AU - Spremo-Potparević, Biljana AU - Đelić, Ninoslav AU - Milicević, Zorana AU - Singh, Avneet K. AU - Fahmy, Lara M. AU - Wang, Xinglong AU - Smith, Mark A. AU - Zhu, Xiongwei PY - 2011 UR - https://vet-erinar.vet.bg.ac.rs/handle/123456789/800 AB - Post-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. PB - BMC, London T2 - Cellular & Molecular Biology Letters T1 - Mislocalization of CDK11/PITSLRE, a regulator of the G2/M phase of the cell cycle, in Alzheimer disease VL - 16 IS - 3 SP - 359 EP - 372 DO - 10.2478/s11658-011-0011-2 ER -
@article{ author = "Bajić, Vladan and Su, Bo and Lee, Hyoung-Gon and Kudo, Wataru and Siedlak, Sandra L. and Živković, Lada and Spremo-Potparević, Biljana and Đelić, Ninoslav and Milicević, Zorana and Singh, Avneet K. and Fahmy, Lara M. and Wang, Xinglong and Smith, Mark A. and Zhu, Xiongwei", year = "2011", abstract = "Post-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.", publisher = "BMC, London", journal = "Cellular & Molecular Biology Letters", title = "Mislocalization of CDK11/PITSLRE, a regulator of the G2/M phase of the cell cycle, in Alzheimer disease", volume = "16", number = "3", pages = "359-372", doi = "10.2478/s11658-011-0011-2" }
Bajić, V., Su, B., Lee, H., Kudo, W., Siedlak, S. L., Živković, L., Spremo-Potparević, B., Đelić, N., Milicević, Z., Singh, A. K., Fahmy, L. M., Wang, X., Smith, M. A.,& Zhu, X.. (2011). Mislocalization of CDK11/PITSLRE, a regulator of the G2/M phase of the cell cycle, in Alzheimer disease. in Cellular & Molecular Biology Letters BMC, London., 16(3), 359-372. https://doi.org/10.2478/s11658-011-0011-2
Bajić V, Su B, Lee H, Kudo W, Siedlak SL, Živković L, Spremo-Potparević B, Đelić N, Milicević Z, Singh AK, Fahmy LM, Wang X, Smith MA, Zhu X. Mislocalization of CDK11/PITSLRE, a regulator of the G2/M phase of the cell cycle, in Alzheimer disease. in Cellular & Molecular Biology Letters. 2011;16(3):359-372. doi:10.2478/s11658-011-0011-2 .
Bajić, Vladan, Su, Bo, Lee, Hyoung-Gon, Kudo, Wataru, Siedlak, Sandra L., Živković, Lada, Spremo-Potparević, Biljana, Đelić, Ninoslav, Milicević, Zorana, Singh, Avneet K., Fahmy, Lara M., Wang, Xinglong, Smith, Mark A., Zhu, Xiongwei, "Mislocalization of CDK11/PITSLRE, a regulator of the G2/M phase of the cell cycle, in Alzheimer disease" in Cellular & Molecular Biology Letters, 16, no. 3 (2011):359-372, https://doi.org/10.2478/s11658-011-0011-2 . .