ArticlePloS one2010
Polo-like kinase 2-dependent phosphorylation of NPM/B23 on serine 4 triggers centriole duplication.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 42 citations in OpenAlex.
- Abnormal PLK2 expression is associated with specific subtypes and may help risk stratification in acute myeloid leukemia.Discover oncology · 2026Article
- Spatio-temporal control of mitosis using light via a Plk1 inhibitor caged for activity and cellular permeability.Nature communications · 2025Article
- Review
- Plk2-mediated phosphorylation and translocalization of Nrf2 activates anti-inflammation through p53/Plk2/p21Cell biology and toxicology · 2023Article
- Polo-Like Kinase 2: From Principle to Practice.Frontiers in oncology · 2022Review
- Review
- Histone Deacetylase SIRT1 Targets Plk2 to Regulate Centriole Duplication.Cell reports · 2018Article
- Non-random aneuploidy specifies subgroups of pilocytic astrocytoma and correlates with older age.Oncotarget · 2015Article
- Cytoplasmic nucleophosmin has elevated T199 phosphorylation upon which G2/M phase progression is dependent.Scientific reports · 2015Article
- Insights into the regulation of neuronal viability by nucleophosmin/B23.Experimental biology and medicine (Maywood, N.J.) · 2015Review
- Functional relationship among PLK2, PLK4 and ROCK2 to induce centrosome amplification.Cell cycle (Georgetown, Tex.) · 2015Article
- Article
- Identification of the PLK2-dependent phosphopeptidome by quantitative proteomics [corrected].PloS one · 2014Article
- Intrinsically disordered regions of nucleophosmin/B23 regulate its RNA binding activity through their inter- and intra-molecular association.Nucleic acids research · 2014Article
- Gene expression analysis in response to osmotic stimuli in the intervertebral disc with DNA microarray.European journal of medical research · 2013Article
- Polo-like kinase 2 regulates selective autophagic α-synuclein clearance and suppresses its toxicity in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Dissection of TBK1 signaling via phosphoproteomics in lung cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- HEXIM1, a New Player in the p53 Pathway.Cancers · 2013Article
- RhoD participates in the regulation of cell-cycle progression and centrosome duplication.Oncogene · 2013Article
- Centrosome dysfunction contributes to chromosome instability, chromoanagenesis, and genome reprograming in cancer.Frontiers in oncology · 2013Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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. We previously reported that Polo-like kinase 2 (Plk2) is activated near the G1/S phase transition, and regulates the reproduction of centrosomes. In search for Plk2 interacting proteins we have identified NPM/B23 (Nucleophosmin) as a novel Plk2 binding partner. We find that Plk2 and NPM/B23 interact in vitro in a Polo-box dependent manner. An association between both proteins was also observed in vivo. Moreover, we show that Plk2 phosphorylates NPM/B23 on serine 4 in vivo in S-phase. Notably, expression of a non-phosphorylatable NPM/B23 S4A mutant interferes with centriole reduplication in S-phase arrested cells and leads to a dilution of centriole numbers in unperturbed U2OS cells. The corresponding phospho-mimicking mutants have the opposite effect and their expression leads to the accumulation of centrioles. These findings suggest that NPM/B23 is a direct target of Plk2 in the regulation of centriole duplication and that phosphorylation on serine 4 can trigger this process.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.