Polo-Like Kinase 2: From Principle to Practice

被引:18
作者
Zhang, Chuanyong [1 ,2 ]
Ni, Chuangye [1 ,2 ]
Lu, Hao [1 ,2 ]
机构
[1] Nanjing Med Univ, Hepatobiliary Ctr, Affiliated Hosp 1, Nanjing, Peoples R China
[2] Chinese Acad Med Sci, Key Lab Liver Transplantat, Nanjing, Peoples R China
关键词
polo-like kinase 2; cell cycle; stress; tumor; neurodegenerative disease; ALPHA-SYNUCLEIN PHOSPHORYLATION; SERINE; 129; PHOSPHORYLATION; ACUTE MYELOID-LEUKEMIA; TRCP UBIQUITIN LIGASE; GENE-EXPRESSION; CENTRIOLE DUPLICATION; PLK2; PHOSPHORYLATES; TUMOR-GROWTH; BOX DOMAIN; IN-VITRO;
D O I
10.3389/fonc.2022.956225
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Polo-like kinase (PLK) 2 is an evolutionarily conserved serine/threonine kinase that shares the n-terminal kinase catalytic domain and the C-terminal Polo Box Domain (PBD) with other members of the PLKs family. In the last two decades, mounting studies have focused on this and tried to clarify its role in many aspects. PLK2 is essential for mitotic centriole replication and meiotic chromatin pairing, synapsis, and crossing-over in the cell cycle; Loss of PLK2 function results in cell cycle disorders and developmental retardation. PLK2 is also involved in regulating cell differentiation and maintaining neural homeostasis. In the process of various stimuli-induced stress, including oxidative and endoplasmic reticulum, PLK2 may promote survival or apoptosis depending on the intensity of stimulation and the degree of cell damage. However, the role of PLK2 in immunity to viral infection has been studied far less than that of other family members. Because PLK2 is extensively and deeply involved in normal physiological functions and pathophysiological mechanisms of cells, its role in diseases is increasingly being paid attention to. The effect of PLK2 in inhibiting hematological tumors and fibrotic diseases, as well as participating in neurodegenerative diseases, has been gradually recognized. However, the research results in solid organ tumors show contradictory results. In addition, preliminary studies using PLK2 as a disease predictor and therapeutic target have yielded some exciting and promising results. More research will help people better understand PLK2 from principle to practice.
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页数:14
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共 172 条
[1]   A Major Diplotaxis harra-Derived Bioflavonoid Glycoside as a Protective Agent against Chemically Induced Neurotoxicity and Parkinson's Models; In Silico Target Prediction; and Biphasic HPTLC-Based Quantification [J].
Ahmed, Atallah F. ;
Wen, Zhi-Hong ;
Bakheit, Ahmed H. ;
Basudan, Omer A. ;
Ghabbour, Hazem A. ;
Al-Ahmari, Abdullah ;
Feng, Chien-Wei .
PLANTS-BASEL, 2022, 11 (05)
[2]   Loss of PLK2 induces acquired resistance to temozolomide in GBM via activation of notch signaling [J].
Alafate, Wahafu ;
Xu, Dongze ;
Wu, Wei ;
Xiang, Jianyang ;
Ma, Xudong ;
Xie, Wanfu ;
Bai, Xiaobin ;
Wang, Maode ;
Wang, Jia .
JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH, 2020, 39 (01)
[3]   A further update on the role of excitotoxicity in the pathogenesis of Parkinson's disease [J].
Ambrosi, Giulia ;
Cerri, Silvia ;
Blandini, Fabio .
JOURNAL OF NEURAL TRANSMISSION, 2014, 121 (08) :849-859
[4]   Regulation of Postsynaptic RapGAP SPAR by Polo-like Kinase 2 and the SCFβ-TRCP Ubiquitin Ligase in Hippocampal Neurons [J].
Ang, Xiaolu L. ;
Seeburg, Daniel P. ;
Sheng, Morgan ;
Harper, J. Wade .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2008, 283 (43) :29424-29432
[5]   Polo-like kinases: conservation and divergence in their functions and regulation [J].
Archambault, Vincent ;
Glover, David M. .
NATURE REVIEWS MOLECULAR CELL BIOLOGY, 2009, 10 (04) :265-275
[6]   Selective and Brain-Permeable Polo-like Kinase-2 (Plk-2) Inhibitors That Reduce -Synuclein Phosphorylation in Rat Brain [J].
Aubele, Danielle L. ;
Hom, Roy K. ;
Adler, Marc ;
Galemmo, Robert A., Jr. ;
Bowers, Simeon ;
Truong, Anh P. ;
Pan, Hu ;
Beroza, Paul ;
Neitz, R. Jeffrey ;
Yao, Nanhua ;
Lin, May ;
Tonn, George ;
Zhang, Heather ;
Bova, Michael P. ;
Ren, Zhao ;
Tam, Danny ;
Ruslim, Lany ;
Baker, Jeanne ;
Diep, Linnea ;
Fitzgerald, Kent ;
Hoffman, Jennifer ;
Motter, Ruth ;
Fauss, Donald ;
Tanaka, Pearl ;
Dappen, Michael ;
Jagodzinski, Jacek ;
Chan, Wayman ;
Konradi, Andrei W. ;
Latimer, Lee ;
Zhu, Yong L. ;
Sham, Hing L. ;
Anderson, John P. ;
Bergeron, Marcelle ;
Artis, Dean R. .
CHEMMEDCHEM, 2013, 8 (08) :1295-1313
[7]   PLK2 Modulates α-Synuclein Aggregation in Yeast and Mammalian Cells [J].
Basso, Elisa ;
Antas, Pedro ;
Marijanovic, Zrinka ;
Goncalves, Susana ;
Tenreiro, Sandra ;
Outeiro, Tiago Fleming .
MOLECULAR NEUROBIOLOGY, 2013, 48 (03) :854-862
[8]   Polo-like kinase 2 (SNK/PLK2) is a novel epigenetically regulated gene in acute myeloid leukemia and myelodysplastic syndromes: genetic and epigenetic interactions [J].
Benetatos, Leonidas ;
Dasoula, Aggeliki ;
Hatzimichael, Eleftheria ;
Syed, Nelofer ;
Voukelatou, Maria ;
Dranitsaris, George ;
Bourantas, Konstantinos L. ;
Crook, Tim .
ANNALS OF HEMATOLOGY, 2011, 90 (09) :1037-1045
[9]   IN VIVO MODULATION OF POLO-LIKE KINASES SUPPORTS A KEY ROLE FOR PLK2 IN SER129 α-SYNUCLEIN PHOSPHORYLATION IN MOUSE BRAIN [J].
Bergeron, M. ;
Motter, R. ;
Tanaka, P. ;
Fauss, D. ;
Babcock, M. ;
Chiou, S. -S. ;
Nelson, S. ;
San Pablo, F. ;
Anderson, J. P. .
NEUROSCIENCE, 2014, 256 :72-82
[10]   Deficient immunoproteasome assembly drives gain of α-synuclein pathology in Parkinson's disease [J].
Bi, Mingxia ;
Du, Xixun ;
Xiao, Xue ;
Dai, Yingying ;
Jiao, Qian ;
Chen, Xi ;
Zhang, Lingqiang ;
Jiang, Hong .
REDOX BIOLOGY, 2021, 47