ArticleOncogene2009
Nucleophosmin protein expression level, but not threonine 198 phosphorylation, is essential in growth and proliferation.
Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- [Overexpression of lncRNA SNHG12 promotes docetaxel resistance of prostate cancer cells by activating PI3K/AKT signalingNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Roniciclib down-regulates stemness and inhibits cell growth by inducing nucleolar stress in neuroblastoma.Scientific reports · 2020Article
- Knockdown of nucleophosmin 1 suppresses proliferation of triple-negative breast cancer cells through activating CDH1/Skp2/p27kip1 pathway.Cancer management and research · 2019Article
- Regulation of Neuronal Survival by Nucleophosmin 1 (NPM1) Is Dependent on Its Expression Level, Subcellular Localization, and Oligomerization Status.The Journal of biological chemistry · 2016Article
- Protein expression of nucleophosmin, annexin A3 and nm23-H1 correlates with human nasopharyngeal carcinoma radioresistanceOncology letters · 2016Article
- Cytoplasmic nucleophosmin has elevated T199 phosphorylation upon which G2/M phase progression is dependent.Scientific reports · 2015Article
- Article
- Phosphorylated STAT3 physically interacts with NPM and transcriptionally enhances its expression in cancer.Oncogene · 2015Article
- Mutual Regulation of FOXM1, NPM and ARF Proteins.Journal of Cancer · 2015Article
- Regulation of subcellular distribution and oncogenic potential of nucleophosmin by plakoglobin.Oncogenesis · 2012Article
- The novel chemical entity YTR107 inhibits recruitment of nucleophosmin to sites of DNA damage, suppressing repair of DNA double-strand breaks and enhancing radiosensitization.Clinical cancer research : an official journal of the American Association for Cancer Research · 2011Article
- Nucleophosmin deposition during mRNA 3' end processing influences poly(A) tail length.The EMBO journal · 2011Article
- Mass spectrometric characterization of protein structure details refines the proteome signature for invasive ductal breast carcinoma.Journal of the American Society for Mass Spectrometry · 2011Article
- The G1 phase Cdks regulate the centrosome cycle and mediate oncogene-dependent centrosome amplification.Cell division · 2011Article
- Identification of FUSE-binding protein 1 as a regulatory mRNA-binding protein that represses nucleophosmin translation.Oncogene · 2011Article
- Effects of salvianolic Acid B on protein expression in human umbilical vein endothelial cells.Evidence-based complementary and alternative medicine : eCAM · 2011Article
- NPM1/B23: A Multifunctional Chaperone in Ribosome Biogenesis and Chromatin Remodeling.Biochemistry research international · 2011Article
- The ARF tumor suppressor regulates bone remodeling and osteosarcoma development in mice.PloS one · 2010Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Nucleophosmin (NPM), an oligomeric phosphoprotein and nucleolar target of the ARF tumor suppressor, contributes to several critical cellular processes. Previous studies have shown that the human NPM's phosphorylation by cyclin E-cyclin-dependent kinase 2 (cdk2) on threonine (Thr) 199 regulates its translocation from the centrosome during cell cycle progression. Given our previous finding that ARF directly binds NPM, impeding its transit to the cytoplasm and arresting cells before S-phase entry, we hypothesized that ARF might also inhibit NPM phosphorylation. However, ARF induction did not impair phosphorylation of the cdk2 target residue in murine NPM, Thr198. Furthermore, phosphorylation of Thr198 occurred throughout the cell cycle and was concomitant with increases in overall NPM expression. To investigate the cell's presumed requirement for NPM-Thr198 phosphorylation in promoting the processes of growth and proliferation, we examined the effects of a non-phosphorylatable NPM mutant, T198A, in a clean cell system in which endogenous NPM had been removed by RNA interference. Here, we show that the T198A mutant is fully capable of executing NPM's described roles in nucleocytoplasmic shuttling, ribosome export and cell cycle progression. Moreover, the proliferative defects observed with stable NPM knockdown were restored by mutant NPM-T198A expression. Thus, we demonstrate that the reduction in NPM protein expression blocks cellular growth and proliferation, whereas phosphorylation of NPM-Thr198 is not essential for NPM's capacity to drive cell cycle progression and proliferation.
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Registered trials
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.