A Role for Polo-Like Kinase 4 in Vascular Fibroblast Cell-Type Transition. [PDF]
Polo-like kinase 4 (PLK4) is canonically known for its cytoplasmic function in centriole duplication. Here we show a noncanonical PLK4 function of regulating the transcription factor SRF's nuclear activity and associated myofibroblast-like cell-type transition.
Li J +8 more
europepmc +3 more sources
Polo-like kinase 4 (PLK4) as a therapeutic target in breast cancer. [PDF]
Abstract Polo-like kinase 4 (PLK4) is a key kinase regulating centriole duplication, centrosome maturation, cytokinesis and other cellular processes. Growing evidence suggests a critical role of PLK4 in the development and progression of various cancers.
Parsyan A, Athwal H, Bhat V, Allan AL.
europepmc +3 more sources
Balancing the scales: fine-tuning Polo-like kinase 4 to ensure proper centriole duplication. [PDF]
Polo-like kinase 4 (Plk4) is the master regulator of centriole assembly. Several evolutionarily conserved mechanisms strictly regulate Plk4 abundance and activity to ensure cells maintain a proper number of centrioles. In this issue of Genes & Development, Phan et al. (pp.
Ryniawec JM, Rogers GC.
europepmc +3 more sources
Polo‑like kinase 4 promotes tumorigenesis and induces resistance to radiotherapy in glioblastoma. [PDF]
Glioblastoma (GBM) is one of the most malignant tumors in adults, associated with severe outcomes (median survival,
Wang J +8 more
europepmc +4 more sources
Polo-like Kinase 4 Shapes Up [PDF]
Polo-like kinase 4 (Plk4) is a master regulator of centriole duplication and targets to centrioles through the association of its cryptic polo box domain with centriole receptors. In this issue of Structure, Shimanovskaya and colleagues unveil a new dimeric architecture of Plk4's cryptic polo box that reveals a conserved mechanism for centriole ...
Levine, Michelle S., Holland, Andrew J.
openaire +2 more sources
Polo-like kinase 4 inhibition: a strategy for cancer therapy? [PDF]
In this issue of Cancer Cell, Mason and colleagues describe the development of a Polo-like kinase 4 (PLK4) inhibitor (CFI-400945), with promising activity against tumors formed in mice from patient-derived tumor tissue. A clinical trial has been initiated, but questions remain as to whether PLK4 is the only relevant therapeutic target.
Holland AJ, Cleveland DW.
europepmc +6 more sources
NFκB regulates expression of Polo-like kinase 4. [PDF]
Activation of the NFκB signaling pathway allows the cell to respond to infection and stress and can affect many cellular processes. As a consequence, NFκB activity must be integrated with a wide variety of parallel signaling pathways. One mechanism through which NFκB can exert widespread effects is through controlling the expression of key regulatory ...
Ledoux AC +5 more
europepmc +4 more sources
Polo-like kinase 2-dependent phosphorylation of NPM/B23 on serine 4 triggers centriole duplication. [PDF]
Duplication of the centrosome is well controlled during faithful cell division while deregulation of this process leads to supernumary centrosomes, chromosome missegregation and aneuploidy, a hallmark of many cancer cells.
Annekatrin Krause, Ingrid Hoffmann
doaj +1 more source
Cell biology. Reversible centriole depletion with an inhibitor of Polo-like kinase 4. [PDF]
Giving an old organelle the old heave-ho Centrioles are ancient cellular organelles that build centrosomes, the major microtubule-organizing centers in animal cells. Duplication of centrioles is tightly controlled to ensure that each dividing cell has precisely two centrosomes.
Wong YL +14 more
europepmc +5 more sources
Tipping the balance: synthesis and evaluation of centrinone-based degraders of polo-like kinase 4. [PDF]
Polo-like kinase 4 (PLK4) is a serine/threonine-protein kinase that plays a pivotal role in centriole biogenesis and, as such, represents a master regulator of centriole duplication. Due to its importance in cancer development and progression, PLK4 represents an attractive target for the development of novel therapeutics.
Kovacevic A +4 more
europepmc +2 more sources

