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Gene Review

PLK3  -  polo-like kinase 3

Homo sapiens

Synonyms: CNK, Cytokine-inducible serine/threonine-protein kinase, FGF-inducible kinase, FNK, PLK-3, ...
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Disease relevance of PLK3


High impact information on PLK3

  • In this study, we fused the protein transduction domain (PTD) of the HIVTat protein to FNK and used the construct in an animal model of ischemic brain injury [4].
  • Assays with the stromal 600-kDa fractions in the presence of the four different nicotinamide-adenine dinucleotides indicate that PRK activity depends on complex dissociation and might be further regulated by the accessible ratio of NADP/NADPH [5].
  • Screening of a pea cDNA library in the yeast two-hybrid system for proteins that interact with CP12, led to the identification of a second member of the Calvin cycle, phosphoribulokinase (PRK; EC, as a further specific binding partner for CP12 [5].
  • Taken together, our studies strongly suggest that Plk3 plays an important role in the regulation of microtubule dynamics and centrosomal function in the cell and that deregulated expression of Plk3 results in cell cycle arrest and apoptosis [6].
  • Human Polo-like kinase 3 (Plk3, previously termed Prk or Fnk) is involved in regulation of cell cycle progression through the M phase (B. Ouyang, H. Pan, L. Lu, J. Li, P. Stambrook, B. Li, and W. Dai, J. Biol. Chem. 272:28646-28651, 1997) [6].

Chemical compound and disease context of PLK3


Biological context of PLK3


Anatomical context of PLK3

  • Furthermore, PLK3(-/-) murine embryonic fibroblast cells exhibited a significantly less fragmentation of the Golgi complex than that in wild-type cells after exposed to nocodazole [10].
  • PLK 1 and PLK3 expression was low in normal ovarian surface epithelium and borderline tumours, with moderately higher expression levels in cystadenomas [1].
  • Among the normal mucosa isolated from rats fed on diets with various levels of fat (LFCO, or high fat diet with corn oil, HFCO, or supplemented with fish oil, HFFO), no significant changes in PLK3 mRNA expression was detected [9].
  • In HeLa cells, although a significant amount of Plk3 signals dispersed in a manner similar to those of Golgi during mitosis concentrated Plk3 was detected at spindle poles, which colocalized with phospho-MEKs and phospho-ERKs [10].
  • We have cloned cDNA fragments of the porcine homologues of Plk1, Plk2, and Plk3 employing fetal fibroblasts as source [11].

Associations of PLK3 with chemical compounds


Physical interactions of PLK3


Regulatory relationships of PLK3

  • Nocodazole activated Plk3 and its activation was blocked by MEK-specific inhibitors (PD98059 or U0126) [10].
  • Furthermore, ectopic expression Chk2 activates cellular Plk3 [16].
  • Interestingly, the Polo box domain of Plk3 is more potent in inhibiting cell proliferation and inducing apoptosis than that of Plk1, suggesting that this domain can provide an additional structural basis for discovery of new anticancer drugs given the current emphasis on Plk1 as a therapeutic target [18].
  • These data show that Plk3 is a RelA-NF-kappaB-regulated gene that induces apoptosis in both p53-dependent and -independent signaling pathways, suggesting a possible mechanism for RelA-NF-kappaB-regulated proapoptotic responses [15].

Co-localisations of PLK3

  • Plk3 co-localized with c-Jun to the nucleus after UV irradiation [19].

Other interactions of PLK3

  • Further, in every case lacking Plk2 expression, there is concomitant overexpression of Plk3, consistent with functional degeneracy between the two proteins [3].
  • Thus, our studies strongly suggest that Plk3 may be a key protein kinase mediating MEK1 function in the Golgi fragmentation pathway during cell division [10].
  • In response to DNA damage, the kinase activity of Plk3 was rapidly increased in an ATM-dependent manner, whereas that of Plk1 was markedly inhibited [12].
  • Furthermore, expression of a kinase-defective Plk3 mutant (Plk3(K52R)) resulted in significant reduction of p53 phosphorylation on serine 20, which was correlated with a decrease in the expression of p21 and with a concomitant increase in cell proliferation [12].
  • Genotoxic stress-induced activation of Plk3 is partly mediated by Chk2 [16].

Analytical, diagnostic and therapeutic context of PLK3


  1. Polo-like kinase isoform expression is a prognostic factor in ovarian carcinoma. Weichert, W., Denkert, C., Schmidt, M., Gekeler, V., Wolf, G., Köbel, M., Dietel, M., Hauptmann, S. Br. J. Cancer (2004) [Pubmed]
  2. Polo-like kinase isoforms in breast cancer: expression patterns and prognostic implications. Weichert, W., Kristiansen, G., Winzer, K.J., Schmidt, M., Gekeler, V., Noske, A., Müller, B.M., Niesporek, S., Dietel, M., Denkert, C. Virchows Arch. (2005) [Pubmed]
  3. Epigenetic inactivation implies a tumor suppressor function in hematologic malignancies for Polo-like kinase 2 but not Polo-like kinase 3. Smith, P., Syed, N., Crook, T. Cell Cycle (2006) [Pubmed]
  4. Protection against ischemic brain injury by protein therapeutics. Asoh, S., Ohsawa, I., Mori, T., Katsura, K., Hiraide, T., Katayama, Y., Kimura, M., Ozaki, D., Yamagata, K., Ohta, S. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  5. CP12 provides a new mode of light regulation of Calvin cycle activity in higher plants. Wedel, N., Soll, J., Paap, B.K. Proc. Natl. Acad. Sci. U.S.A. (1997) [Pubmed]
  6. Cell cycle arrest and apoptosis induced by human Polo-like kinase 3 is mediated through perturbation of microtubule integrity. Wang, Q., Xie, S., Chen, J., Fukasawa, K., Naik, U., Traganos, F., Darzynkiewicz, Z., Jhanwar-Uniyal, M., Dai, W. Mol. Cell. Biol. (2002) [Pubmed]
  7. The effect of early steroid treatment after PRK on clinical and refractive outcomes. Vetrugno, M., Maino, A., Quaranta, G.M., Cardia, L. Acta ophthalmologica Scandinavica. (2001) [Pubmed]
  8. A comparative study of epithelial hyperplasia after PRK: Summit versus VISX in the same patient. Hamberg-Nyström, H., Gauthier, C.A., Holden, B.A., Epstein, D., Fagerholm, P., Tengroth, B. Acta ophthalmologica Scandinavica. (1996) [Pubmed]
  9. Down-regulation of PLK3 gene expression by types and amount of dietary fat in rat colon tumors. Dai, W., Liu, T., Wang, Q., Rao, C.V., Reddy, B.S. Int. J. Oncol. (2002) [Pubmed]
  10. MEK1-induced Golgi dynamics during cell cycle progression is partly mediated by Polo-like kinase-3. Xie, S., Wang, Q., Ruan, Q., Liu, T., Jhanwar-Uniyal, M., Guan, K., Dai, W. Oncogene (2004) [Pubmed]
  11. Cell cycle dependent expression of Plk1 in synchronized porcine fetal fibroblasts. Anger, M., Kues, W.A., Klima, J., Mielenz, M., Kubelka, M., Motlik, J., Esner, M., Dvorak, P., Carnwath, J.W., Niemann, H. Mol. Reprod. Dev. (2003) [Pubmed]
  12. Plk3 functionally links DNA damage to cell cycle arrest and apoptosis at least in part via the p53 pathway. Xie, S., Wu, H., Wang, Q., Cogswell, J.P., Husain, I., Conn, C., Stambrook, P., Jhanwar-Uniyal, M., Dai, W. J. Biol. Chem. (2001) [Pubmed]
  13. Polo-like Kinases Inhibited by Wortmannin: LABELING SITE AND DOWNSTREAM EFFECTS. Liu, Y., Jiang, N., Wu, J., Dai, W., Rosenblum, J.S. J. Biol. Chem. (2007) [Pubmed]
  14. Intron/exon organization and polymorphisms of the PLK3/PRK gene in human lung carcinoma cell lines. Wiest, J., Clark, A.M., Dai, W. Genes Chromosomes Cancer (2001) [Pubmed]
  15. Function of polo-like kinase 3 in NF-kappaB-mediated proapoptotic response. Li, Z., Niu, J., Uwagawa, T., Peng, B., Chiao, P.J. J. Biol. Chem. (2005) [Pubmed]
  16. Genotoxic stress-induced activation of Plk3 is partly mediated by Chk2. Xie, S., Wu, H., Wang, Q., Kunicki, J., Thomas, R.O., Hollingsworth, R.E., Cogswell, J., Dai, W. Cell Cycle (2002) [Pubmed]
  17. Physical and functional interactions between mitotic kinases during polyploidization and megakaryocytic differentiation. Huang, X., Ruan, Q., Fang, Y., Traganos, F., Darzynkiewicz, Z., Dai, W. Cell Cycle (2004) [Pubmed]
  18. Polo box domain of Plk3 functions as a centrosome localization signal, overexpression of which causes mitotic arrest, cytokinesis defects, and apoptosis. Jiang, N., Wang, X., Jhanwar-Uniyal, M., Darzynkiewicz, Z., Dai, W. J. Biol. Chem. (2006) [Pubmed]
  19. Stress-induced c-Jun activation mediated by Polo-like kinase 3 in corneal epithelial cells. Wang, L., Dai, W., Lu, L. J. Biol. Chem. (2007) [Pubmed]
  20. PRK, a cell cycle gene localized to 8p21, is downregulated in head and neck cancer. Dai, W., Li, Y., Ouyang, B., Pan, H., Reissmann, P., Li, J., Wiest, J., Stambrook, P., Gluckman, J.L., Noffsinger, A., Bejarano, P. Genes Chromosomes Cancer (2000) [Pubmed]
  21. LASIK and PRK malpractice predictors. Probst, L.E. Ophthalmology (2004) [Pubmed]
  22. PRK retreatments after regressed myopic LASIK. Yavitz, E. Ophthalmology (2002) [Pubmed]
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