Browse by author
Lookup NU author(s): Dr Adeline Ledoux,
Dr Alessio Iannetti,
Professor Neil PerkinsORCiD
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License (CC BY-NC 4.0).
Activation of the NF kappa B signaling pathway allows the cell to respond to infection and stress and can affect many cellular processes. As a consequence, NF kappa B activity must be integrated with a wide variety of parallel signaling pathways. One mechanism through which NF kappa B can exert widespread effects is through controlling the expression of key regulatory kinases. Here we report that NF kappa B regulates the expression of genes required for centrosome duplication, and that Polo-like kinase 4 (PLK4) is a direct NF kappa B target gene. RNA interference, chromatin immunoprecipitation, and analysis of the PLK4 promoter in a luciferase reporter assay revealed that all NF kappa B subunits participate in its regulation. Moreover, we demonstrate that NF kappa B regulation of PLK4 expression is seen in multiple cell types. Significantly long-term deletion of the NF kappa B2 (p100/p52) subunit leads to defects in centrosome structure. This data reveals a new component of cell cycle regulation by NF kappa B and suggests a mechanism through which deregulated NF kappa B activity in cancer can lead to increased genomic instability and uncontrolled proliferation.
Author(s): Ledoux AC, Sellier H, Gillies K, Iannetti A, James J, Perkins ND
Publication type: Article
Publication status: Published
Journal: Cell Cycle
Print publication date: 21/08/2013
Date deposited: 07/07/2015
ISSN (print): 1538-4101
ISSN (electronic): 1551-4005
Publisher: Landes Bioscience
Altmetrics provided by Altmetric