TY  - JOUR
AU  - Bajić, Vladan
AU  - Su, Bo
AU  - Lee, Hyoung-Gon
AU  - Kudo, Wataru
AU  - Siedlak, Sandra L.
AU  - Živković, Lada
AU  - 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://farfar.pharmacy.bg.ac.rs/handle/123456789/1554
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 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., 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, 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, 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 . .

TY  - JOUR
AU  - Bonda, David J.
AU  - Bajić, Vladan
AU  - Potparević, Biljana
AU  - Casadesus, G.
AU  - Zhu, Xiongwei
AU  - Smith, Mark A.
AU  - Lee, Hyoung-Gon
PY  - 2010
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/1378
AB  - The cell cycle is a highly regulated and fundamental cellular process that involves complex feedback regulation of many proteins, and any compromise to its integrity elicits dire consequences for the cell. For example, in neurodegenerative diseases such as Alzheimer disease (AD), evidence for abnormal cell cycle re-entry precedes other hallmarks of disease and as such, implicates cell cycle aberrations in the aetiology of AD. The mechanism(s) for cell cycle re-entry in AD, however, remain unclear. Current theory suggests it to be part of a combination of early events that together elicit the degenerative pathology and cognitive phenotype consistent with the disease. We propose a 'Two-Hit Hypothesis' that highlights the concerted interaction between cell cycle alterations and oxidative stress that combine to produce neurodegeneration. Here, we review the evidence implicating cell cycle mechanisms in AD and how such changes, especially in combination with oxidative stress, would lead to a cascade of events leading to disease. Based on this concept, we propose new opportunities for disease treatment.
PB  - Wiley, Hoboken
T2  - Neuropathology and Applied Neurobiology
T1  - Review: Cell cycle aberrations and neurodegeneration
VL  - 36
IS  - 2
SP  - 157
EP  - 163
DO  - 10.1111/j.1365-2990.2010.01064.x
ER  - 

@article{
author = "Bonda, David J. and Bajić, Vladan and Potparević, Biljana and Casadesus, G. and Zhu, Xiongwei and Smith, Mark A. and Lee, Hyoung-Gon",
year = "2010",
abstract = "The cell cycle is a highly regulated and fundamental cellular process that involves complex feedback regulation of many proteins, and any compromise to its integrity elicits dire consequences for the cell. For example, in neurodegenerative diseases such as Alzheimer disease (AD), evidence for abnormal cell cycle re-entry precedes other hallmarks of disease and as such, implicates cell cycle aberrations in the aetiology of AD. The mechanism(s) for cell cycle re-entry in AD, however, remain unclear. Current theory suggests it to be part of a combination of early events that together elicit the degenerative pathology and cognitive phenotype consistent with the disease. We propose a 'Two-Hit Hypothesis' that highlights the concerted interaction between cell cycle alterations and oxidative stress that combine to produce neurodegeneration. Here, we review the evidence implicating cell cycle mechanisms in AD and how such changes, especially in combination with oxidative stress, would lead to a cascade of events leading to disease. Based on this concept, we propose new opportunities for disease treatment.",
publisher = "Wiley, Hoboken",
journal = "Neuropathology and Applied Neurobiology",
title = "Review: Cell cycle aberrations and neurodegeneration",
volume = "36",
number = "2",
pages = "157-163",
doi = "10.1111/j.1365-2990.2010.01064.x"
}

Bonda, D. J., Bajić, V., Potparević, B., Casadesus, G., Zhu, X., Smith, M. A.,& Lee, H.. (2010). Review: Cell cycle aberrations and neurodegeneration. in Neuropathology and Applied Neurobiology
Wiley, Hoboken., 36(2), 157-163.
https://doi.org/10.1111/j.1365-2990.2010.01064.x

Bonda DJ, Bajić V, Potparević B, Casadesus G, Zhu X, Smith MA, Lee H. Review: Cell cycle aberrations and neurodegeneration. in Neuropathology and Applied Neurobiology. 2010;36(2):157-163.
doi:10.1111/j.1365-2990.2010.01064.x .

Bonda, David J., Bajić, Vladan, Potparević, Biljana, Casadesus, G., Zhu, Xiongwei, Smith, Mark A., Lee, Hyoung-Gon, "Review: Cell cycle aberrations and neurodegeneration" in Neuropathology and Applied Neurobiology, 36, no. 2 (2010):157-163,
https://doi.org/10.1111/j.1365-2990.2010.01064.x . .