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Polo-like kinase 4

SAK, Plk4
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. Three alternatively spliced transcript variants that encode different protein isoforms have been found for this gene. [provided by RefSeq, Jun 2010] (from NCBI)
Top mentioned proteins: CAN, Plasminogen, Plk1, ACID, HAD
Papers using SAK antibodies
Sak serine-threonine kinase acts as an effector of Tec tyrosine kinase
Cleveland Don W. et al., In The Journal of Cell Biology, 2000
... A fragment of mouse Plk4 (aa 223–387) encoding the appropriate mutations was synthesized (Genscript) and used to replace ...
Papers on SAK
The E2F-DP1 Transcription Factor Complex Regulates Centriole Duplication in C. elegans.
O'Connell et al., In G3 (bethesda), Feb 2016
Recent studies have revealed that post-translational control of the master regulator Plk4/ZYG-1 kinase and its downstream effector SAS-6 is key to ensuring production of a single daughter centriole.
A non-canonical function of Plk4 in centriolar satellite integrity and ciliogenesis through PCM1 phosphorylation.
Toda et al., Ikoma, Japan. In Embo Rep, Feb 2016
UNASSIGNED: Centrioles are the major constituents of the animal centrosome, in which Plk4 kinase serves as a master regulator of the duplication cycle.
Transient PLK4 overexpression accelerates tumorigenesis in p53-deficient epidermis.
Blanpain et al., Brussels, Belgium. In Nat Cell Biol, Jan 2016
Using Plk4 overexpression (PLK4OE) during epidermal development, we assess the impact of centrosome amplification and aneuploidy on skin development and tumorigenesis.
Conserved molecular interactions in centriole-to-centrosome conversion.
Glover et al., Siena, Italy. In Nat Cell Biol, Jan 2016
This conserved architectural framework is essential for loading Asterless or Cep152, the partner of the master regulator of centriole duplication, Plk4.
Over-expression of Plk4 induces centrosome amplification, loss of primary cilia and associated tissue hyperplasia in the mouse.
Glover et al., Cambridge, United Kingdom. In Open Biol, Dec 2015
To address the long-known relationship between supernumerary centrosomes and cancer, we have generated a transgenic mouse that permits inducible expression of the master regulator of centriole duplication, Polo-like-kinase-4 (Plk4).
Targeting Mitosis in Cancer: Emerging Strategies.
Mak et al., Toronto, Canada. In Mol Cell, Dec 2015
This reasoning stimulated our development of novel inhibitors targeting the critical regulators of genomic stability and the mitotic checkpoint: AURKA, PLK4, and Mps1/TTK.
Chronic centrosome amplification without tumorigenesis.
Cleveland et al., San Diego, United States. In Proc Natl Acad Sci U S A, Dec 2015
To do this, we constructed and analyzed mice in which centrosome amplification can be induced by a Cre-recombinase-mediated increase in expression of Polo-like kinase 4 (Plk4).
Epidermal development, growth control, and homeostasis in the face of centrosome amplification.
Fuchs et al., Montpellier, France. In Proc Natl Acad Sci U S A, Dec 2015
Here we addressed this issue by generating a mouse model inducing centrosome amplification in a naturally proliferative epithelial tissue by elevating Polo-like kinase 4 (Plk4) expression in the skin epidermis.
What next-generation sequencing (NGS) technology has enabled us to learn about primary autosomal recessive microcephaly (MCPH).
Kaindl et al., London, United Kingdom. In Mol Cell Probes, Oct 2015
The functions of proteins such as WDR62, CASC5, PHC1, CDK6, CENP-E, CENP-F, CEP63, ZNF335, PLK4 and TUBGPC, have been added to the complex network of critical cellular processes known to be involved in brain growth and size.
Cell biology. Reversible centriole depletion with an inhibitor of Polo-like kinase 4.
Oegema et al., San Diego, United States. In Science, Jul 2015
To investigate the importance of centrosomes in the proliferation of normal and cancer cells, we developed centrinone, a reversible inhibitor of Polo-like kinase 4 (Plk4), a serine-threonine protein kinase that initiates centriole assembly.
Targeting Polo-Like Kinases: A Promising Therapeutic Approach for Cancer Treatment.
Liu, West Lafayette, United States. In Transl Oncol, Jun 2015
Other Plk inhibitors, including the Plk1 inhibitors GSK461364A, TKM-080301, GW843682, purpurogallin, and poloxin and the Plk4 inhibitor CFI-400945 fumarate, are in earlier clinical development.
Discovery of orally active anticancer candidate CFI-400945 derived from biologically promising spirooxindoles: success and challenges.
Liu et al., Zhengzhou, China. In Eur J Med Chem, Jun 2015
Among spirooxindoles, CFI-400945 holds its promise as the first potent PLK4 inhibitor, the fumarate of CFI-400945 has entered phase I clinical trials for the treatment of solid tumors.
Common variants spanning PLK4 are associated with mitotic-origin aneuploidy in human embryos.
Petrov et al., Stanford, United States. In Science, May 2015
This associated region contains a candidate gene, Polo-like kinase 4 (PLK4), that plays a well-characterized role in centriole duplication and has the ability to alter mitotic fidelity upon minor dysregulation.
Expression and characterization of bifunctional fusion proteins possessing antitumor and thrombolytic function for targeting therapy.
Hu et al., Shenyang, China. In Biotechnol Appl Biochem, Mar 2015
After expression and purification, fusion proteins could significantly stimulate proliferation of mouse spleen lymphocyte, obviously inhibit the growth of human gastric carcinoma BGC-823, and have thrombolytic activity, indicating that fusion proteins retained bioactivities of staphylococcal enterotoxin C2 and Sak.
Mutations in PLK4, encoding a master regulator of centriole biogenesis, cause microcephaly, growth failure and retinopathy.
Jackson et al., Köln, Germany. In Nat Genet, 2014
Here we identify mutations in the genes encoding PLK4 kinase, a master regulator of centriole duplication, and its substrate TUBGCP6 in individuals with microcephalic primordial dwarfism and additional congenital anomalies, including retinopathy, thereby extending the human phenotypic spectrum associated with centriole dysfunction.
Polo-like kinase 4 controls centriole duplication but does not directly regulate cytokinesis.
Cleveland et al., San Diego, United States. In Mol Biol Cell, 2012
Plk4 is a centriole-localized kinase that does not directly regulate cytokinesis.
Cell-cycle-regulated expression of STIL controls centriole number in human cells.
Nigg et al., Basel, Switzerland. In J Cell Sci, 2012
STIL cooperates with SAS-6 and PLK4 in the control of centriole number and represents a key centriole duplication factor in human cells.
The Protein Phosphatase 2A regulatory subunit Twins stabilizes Plk4 to induce centriole amplification.
Rogers et al., Tucson, United States. In J Cell Biol, 2011
PP2A (Protein Phosphatase 2A(Twins)) counteracts Plk4 autophosphorylation, thus stabilizing Plk4 and promoting centriole duplication
Male hypogonadism and germ cell loss caused by a mutation in Polo-like kinase 4.
Jameson et al., Chicago, United States. In Endocrinology, 2011
the I242N heterozygous mutation in PLK4 is causative for patchy germ cell loss beginning at P10, suggesting a role for PLK4 during the initiation of spermatogenesis.
The SCF-FBXW5 E3-ubiquitin ligase is regulated by PLK4 and targets HsSAS-6 to control centrosome duplication.
Malek et al., Hannover, Germany. In Nat Cell Biol, 2011
The activity of SCF-FBXW5 is negatively regulated by Polo-like kinase 4 (PLK4), which phosphorylates FBXW5 at Ser 151 to suppress its ability to ubiquitylate HsSAS-6.
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