PLK4

From Wikipedia, the free encyclopedia
Jump to: navigation, search
Polo-like kinase 4
Protein PLK4 PDB 1mby.png
PDB rendering based on 1mby.
Available structures
PDB Ortholog search: PDBe, RCSB
Identifiers
Symbols PLK4 ; SAK; STK18
External IDs OMIM605031 MGI101783 HomoloGene7962 ChEMBL: 3788 GeneCards: PLK4 Gene
EC number 2.7.11.21
RNA expression pattern
PBB GE PLK4 204887 s at tn.png
PBB GE PLK4 204886 at tn.png
PBB GE PLK4 211088 s at tn.png
More reference expression data
Orthologs
Species Human Mouse
Entrez 10733 20873
Ensembl ENSG00000142731 ENSMUSG00000025758
UniProt O00444 Q64702
RefSeq (mRNA) NM_001190799 NM_011495
RefSeq (protein) NP_001177728 NP_035625
Location (UCSC) Chr 4:
128.8 – 128.82 Mb
Chr 3:
40.8 – 40.82 Mb
PubMed search [1] [2]

Serine/threonine-protein kinase PLK4 also known as polo-like kinase 4 is an enzyme that in humans is encoded by the PLK4 gene.[1]

Function[edit]

This gene encodes a member of the polo family of serine/threonine protein kinases. The protein localizes to centrioles, complex microtubule-based structures found in centrosomes, and regulates centriole duplication during the cell cycle.[1]

As a cancer drug target[edit]

Inhibitors of the enzymatic activity PLK4 have potential in the treatment of cancer.[2] The PLK4 inhibitor R1530 down regulates the expression of mitotic checkpoint kinase BubR1 that in turn leads to polyploidy rendering cancer cells unstable and more sensitive to cancer chemotherapy. Furthermore normal cells are resistant to the polyploidy inducing effects of R1530.[3]

Another PLK4 inhibitor, CFI-400945 has demonstrated efficacy in animal models of breast and ovarian cancer.[4]

Interactions[edit]

PLK4 has been shown to interact with Stratifin.[5]

References[edit]

  1. ^ a b "Entrez Gene: PLK4 polo-like kinase 4 (Drosophila)". 
  2. ^ Mason J, Wei S, Luo X, Nadeem V, Kiarash R, Huang P, Awrey D, Leung G, Beletskaya I, Feher M, Forrest B, Laufer R, Sampson P, Li S-W, Liu Y, Lang Y, Pauls H, Mak T, Pan JG. "Inhibition of Polo-like kinase 4 as an anti-cancer strategy". Abstract LB-215. Cancer Research. pp. LB–215. 
  3. ^ Tovar C, Higgins B, Deo D, Kolinsky K, Liu JJ, Heimbrook DC, Vassilev LT (August 2010). "Small-molecule inducer of cancer cell polyploidy promotes apoptosis or senescence: Implications for therapy". Cell Cycle 9 (16): 3364–75. doi:10.4161/cc.9.16.12732. PMID 20814247. 
  4. ^ "Experimental drug shows promise in treating breast, ovarian cancer". News. Canadian Broadcasting Corporation. 2013-06-18. 
  5. ^ Rual JF, Venkatesan K, Hao T, Hirozane-Kishikawa T, Dricot A, Li N, Berriz GF, Gibbons FD, Dreze M, Ayivi-Guedehoussou N, Klitgord N, Simon C, Boxem M, Milstein S, Rosenberg J, Goldberg DS, Zhang LV, Wong SL, Franklin G, Li S, Albala JS, Lim J, Fraughton C, Llamosas E, Cevik S, Bex C, Lamesch P, Sikorski RS, Vandenhaute J, Zoghbi HY, Smolyar A, Bosak S, Sequerra R, Doucette-Stamm L, Cusick ME, Hill DE, Roth FP, Vidal M (October 2005). "Towards a proteome-scale map of the human protein-protein interaction network". Nature 437 (7062): 1173–8. doi:10.1038/nature04209. PMID 16189514. 

Further reading[edit]