Affinage

NPM1

Nucleophosmin · UniProt P06748

Length
294 aa
Mass
32.6 kDa
Annotated
2026-04-29
100 papers in source corpus 34 papers cited in narrative 34 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

NPM1 is a multifunctional nucleolar phosphoprotein that integrates ribosome biogenesis, centrosome duplication, p53 regulation, and transcriptional control. It possesses intrinsic ribonuclease activity for pre-rRNA processing and molecular chaperone activity that prevents protein aggregation and promotes refolding, while also chaperoning NF-κB p65 to enhance its DNA-binding capacity (PMID:7479045, PMID:10211837, PMID:28003476). NPM1 governs centrosome duplication through CDK2/cyclin E-mediated Thr199 phosphorylation that recruits ROCK II, Plk1-mediated Ser4 phosphorylation during mitosis, and Plk2-mediated Ser4 phosphorylation during S-phase, while Aurora kinase phosphorylation at Ser125 directs its midbody localization for cytokinesis (PMID:17015463, PMID:15190079, PMID:20352051, PMID:24857377). NPM1 controls p53 stability by sequestering ARF in the nucleolus — an interaction disrupted by DNA damage to permit ARF–MDM2 complex formation — and via SIRT7-dependent deacetylation that triggers NPM1 translocation to the nucleoplasm where it binds MDM2 and blocks p53 ubiquitination; the leukemia-associated cytoplasmic mutant NPM1c acquires a neomorphic chromatin-binding function at HOXA/B and MEIS1 loci in cooperation with MLL1, and its cytoplasmic localization is required to maintain the AML leukemic state (PMID:14729947, PMID:16267006, PMID:33495326, PMID:36455613, PMID:30205049).

Mechanistic history

Synthesis pass · year-by-year structured walk · 26 steps
  1. 1992 Medium

    Establishing that NPM1 undergoes reversible nucleolar-to-nucleoplasm translocation in response to cytotoxic stress, without requiring new protein synthesis, defined NPM1 as a dynamically shuttling protein whose localization is functionally regulated.

    Evidence Drug washout with cycloheximide, immunolocalization, and oligomeric/phosphorylation state analysis

    PMID:1426041

    Open questions at the time
    • Single-lab study without genetic perturbation
    • Molecular signals driving relocation were not identified
    • Whether translocation has functional consequences beyond redistribution was unknown
  2. 1995 High

    Demonstration that NPM1 possesses intrinsic ribonuclease activity with isoform-specific differences (B23.1 > B23.2) established a direct enzymatic role in pre-rRNA processing, moving beyond its prior characterization as merely an abundant nucleolar protein.

    Evidence RNA-embedded gel assay and perchloric acid precipitation with purified recombinant B23.1 and B23.2

    PMID:7479045

    Open questions at the time
    • Specific rRNA cleavage sites were not mapped
    • In vivo relevance of the ribonuclease activity was not demonstrated
  3. 1996 High

    Identification of NPM1 as a nucleolar-localization-signal-binding protein that interacts with nucleolin and p120 through a defined domain revealed how NPM1 organizes nucleolar architecture by anchoring other nucleolar residents.

    Evidence Yeast two-hybrid with deletion mapping confirmed by co-immunoprecipitation from HeLa nuclear extract

    PMID:8620867

    Open questions at the time
    • Whether NPM1 actively imports these partners or simply retains them in the nucleolus was not resolved
    • Stoichiometry and dynamics of the complexes were not determined
  4. 1997 Medium

    Systematic mapping of NPM1's cell-cycle-dependent localization — nucleolar in interphase, perichromosomal during mitosis, and in prenucleolar bodies at telophase — provided the spatial framework for understanding its diverse mitotic functions.

    Evidence Immunofluorescence across three cell lines with Triton/RNase extraction and SDS-PAGE mobility shift analysis

    PMID:9174672

    Open questions at the time
    • No direct functional perturbation at specific mitotic stages
    • Kinases responsible for mitotic phosphorylation were not identified at this time
  5. 1997 High

    Proof that the NPM-ALK fusion is a direct causative oncogene sufficient to induce lymphoma in vivo established the pathogenic consequence of the t(2;5) translocation involving NPM1.

    Evidence Retroviral NPM-ALK expression in bone marrow transplant with clonal B-cell lymphoma and secondary transplantation

    PMID:9376569

    Open questions at the time
    • Downstream signaling pathways were not dissected
    • Why the fusion produces B-lineage rather than T-lineage lymphoma in this model was unexplained
  6. 1999 High

    Demonstration that NPM1 functions as a general molecular chaperone — preventing aggregation, protecting enzymatic activity, and promoting refolding of diverse substrates — established a biochemical activity underlying many of its cellular roles.

    Evidence In vitro aggregation, activity protection, and refolding assays with multiple substrates

    PMID:10211837

    Open questions at the time
    • In vivo chaperone substrates were not identified
    • Relationship between chaperone and ribonuclease activities was not addressed
  7. 2004 High

    Discovery that ARF physically associates with NPM1 in high-molecular-weight complexes and requires this interaction to retard rRNA processing — while DNA damage disrupts the ARF–NPM1 complex to liberate ARF for p53-pathway activation — unified NPM1's roles in ribosome biogenesis and tumor suppression.

    Evidence TAP purification, co-immunoprecipitation, sucrose gradient sedimentation, dominant-negative NPM1 mutant in multiple cell types; UV/gamma irradiation time-course with co-IP and immunofluorescence

    PMID:14729947 PMID:15485902 PMID:16267006

    Open questions at the time
    • How DNA damage signals mechanistically disrupt the ARF–NPM1 interface was not defined
    • Whether ARF-independent rRNA processing functions of NPM1 are affected by damage was not tested
  8. 2004 High

    Identification of Plk1 as the mitotic kinase phosphorylating NPM1 at Ser4, with S4A mutation causing centrosome and cytokinesis defects, provided the first kinase–substrate link explaining NPM1's essential role in mitotic centrosome regulation.

    Evidence In vitro/in vivo kinase assays, Plk1 kinase-dead and constitutively-active mutants, RNAi, S4A mutant phenotyping

    PMID:15190079

    Open questions at the time
    • How Ser4 phosphorylation alters NPM1 protein interactions at centrosomes was unknown
    • Whether other Plk family members contribute during other cell-cycle phases was not tested
  9. 2005 High

    Discovery that PARP-1 and PARP-2 constitutively interact with NPM1 through their DNA-binding domains and co-delocalize upon RNA Pol I inhibition linked NPM1 to the DNA damage and chromatin repair machinery within the nucleolus.

    Evidence Reciprocal co-immunoprecipitation, NLS mutagenesis, RNA Pol I inhibition with colocalization

    PMID:15615785

    Open questions at the time
    • Functional consequence of the PARP–NPM1 interaction for DNA repair or rDNA transcription was not determined
    • Whether poly(ADP-ribosyl)ation of NPM1 occurs was not tested
  10. 2006 High

    Demonstration that ROCK II localizes to centrosomes, is activated by NPM1 binding (enhanced by CDK2-mediated Thr199 phosphorylation), and controls centrosome duplication established ROCK II as a downstream effector in the CDK2–NPM1 centrosome licensing pathway.

    Evidence Co-immunoprecipitation, kinase activity assay, siRNA and constitutively active ROCK II with centrosome counting

    PMID:17015463

    Open questions at the time
    • ROCK II substrates at the centrosome were not identified
    • Whether ROCK II acts on NPM1 itself or on other centrosomal targets was not resolved
  11. 2007 High

    Mapping NPM1 sumoylation at Lys263 as a master switch controlling centrosomal/nucleolar residency, Rb binding, E2F1-driven transcription, and caspase-3 resistance revealed how a single post-translational modification integrates NPM1's roles in proliferation, localization, and apoptosis.

    Evidence Site-directed mutagenesis of K263 and K230, Co-IP with Rb, E2F1 reporter assay, caspase-3 cleavage assay, PI(3,4,5)P3 binding

    PMID:17535915

    Open questions at the time
    • SUMO E3 ligase responsible for K263 modification was not identified
    • How sumoylation structurally alters NPM1 to expose Rb-binding surface was unknown
  12. 2007 High

    Identification of NPM1–Ebp1 complexes with differential sumoylation and phosphorylation requirements linked NPM1 post-translational modifications to ribosome biogenesis output and cell survival.

    Evidence Co-immunoprecipitation with sumoylation-deficient NPM1 and phospho-mutant Ebp1/p42, siRNA, ribosome biogenesis and viability assays

    PMID:17951246

    Open questions at the time
    • Which specific ribosomal assembly step is regulated by NPM1–Ebp1 was not defined
    • Whether EGF-dependent p42 recruitment has physiological relevance beyond cell culture was untested
  13. 2008 High

    Demonstration that Npm1 heterozygous mice develop myeloid and lymphoid malignancies without loss of the remaining allele established NPM1 as a haploinsufficient tumor suppressor in the hematopoietic system.

    Evidence Npm1+/- knockout mouse model with longitudinal tumor surveillance and immunohistochemistry

    PMID:18212245

    Open questions at the time
    • Which NPM1-dependent pathway(s) are rate-limiting at half dosage was not determined
    • Whether haploinsufficiency cooperates with specific secondary mutations was not systematically tested
  14. 2009 High

    Demonstration that NPM1 directly binds and stabilizes p21 by inhibiting its ubiquitination added a second, ARF-independent mechanism by which NPM1 enforces cell-cycle checkpoints.

    Evidence Reciprocal co-immunoprecipitation, GST pull-down, pulse-chase half-life, ubiquitination assay, siRNA

    PMID:19221506

    Open questions at the time
    • The E3 ubiquitin ligase antagonized by NPM1 was not identified
    • Whether this mechanism operates during DNA damage or only at steady state was not tested
  15. 2009 High

    Dissection of NPM-ALK signaling showed that the fusion inactivates p53 through JNK-dependent and MDM2-dependent mechanisms while excluding p53 from the nucleus via PI3K, explaining how ALK-driven lymphomas evade tumor suppression.

    Evidence ALK kinase inhibition, JNK/PI3K/MDM2 inhibitors, p53 immunofluorescence and apoptosis assays

    PMID:19286999

    Open questions at the time
    • Direct phosphorylation targets linking ALK to JNK activation were not mapped
    • Whether p53 reactivation is sufficient for durable anti-tumor responses was not tested
  16. 2010 High

    Discovery that Plk2 phosphorylates NPM1 at Ser4 during S-phase to license centriole reduplication resolved the question of which kinase controls NPM1's centrosome role outside mitosis, complementing the Plk1 finding.

    Evidence In vitro kinase assay with Polo-box domain interaction, co-immunoprecipitation, S4A/S4D mutant centriole counting

    PMID:20352051

    Open questions at the time
    • Whether Plk1 and Plk2 phosphorylation of S4 have distinct downstream effects was not compared
    • How S4 phosphorylation alters NPM1 interaction with centrosomal substrates was not defined
  17. 2011 High

    Identification of GSK3β as a critical NPM-ALK effector — inactivated by ALK-driven PI3K/AKT phosphorylation to stabilize Mcl-1 and CDC25A — defined a targetable survival axis in ALK-positive lymphoma.

    Evidence Phosphoproteomic screen, ALK inhibitor, kinase-dead NPM-ALK, GSK3β siRNA/inhibitor rescue

    PMID:22179823

    Open questions at the time
    • Whether GSK3β reactivation alone is sufficient for lymphoma regression was not tested in vivo
    • Other GSK3β substrates relevant to ALK-driven transformation were not catalogued
  18. 2014 High

    Discovery of Aurora A/B phosphorylation of NPM1 at Ser125, with phospho-S125 localizing to the midbody and S125A causing cytokinesis failure, established a third mitotic kinase input controlling NPM1's function in cell division completion.

    Evidence In vitro kinase assay, phospho-specific antibody, immunofluorescence, S125A mutant with mitotic phenotype analysis

    PMID:24857377

    Open questions at the time
    • What NPM1 does at the midbody mechanistically was not determined
    • Whether S125 phosphorylation is coordinated with S4 or T199 phosphorylation was not examined
  19. 2015 High

    Demonstration that CD24 competitively displaces ARF from NPM1, leading to ARF degradation and p53 pathway suppression, revealed an upstream regulator of the NPM1–ARF–p53 axis.

    Evidence Competitive co-immunoprecipitation, CD24 shRNA/mutation, Western blot for pathway components, viral oncogene rescue

    PMID:25600590

    Open questions at the time
    • Structural basis for CD24–NPM1 competition with ARF was not determined
    • Whether CD24 regulation of this axis operates in normal physiology or only in cancer was unclear
  20. 2016 High

    Revealing that endogenous NPM1 heterodimerizes with and inactivates nuclear NPM-ALK in ALCL, while only cytoplasmic NPM-ALK is catalytically active, explained how NPM1 dosage controls oncogenic ALK signaling strength.

    Evidence Nuclear/cytoplasmic fractionation, kinase activity assay, NPM1 siRNA/KO, co-immunoprecipitation, DNA damage markers

    PMID:26657151

    Open questions at the time
    • Whether therapeutic strategies increasing nuclear NPM-ALK:NPM1 ratio could be beneficial was not tested
    • Stoichiometry of heterodimer versus homodimer pools was not quantified
  21. 2017 High

    Discovery that NPM1 enhances NF-κB p65 DNA-binding activity through a chaperone-like mechanism — without becoming part of the DNA complex — and is required for inflammatory gene expression extended NPM1's chaperone function to transcription factor activation.

    Evidence Co-immunoprecipitation, ChIP, siRNA knockdown, luciferase reporter, invasion assay in breast cancer cells

    PMID:28003476

    Open questions at the time
    • Whether NPM1 similarly chaperones other transcription factors beyond p65 was not systematically tested
    • The structural basis for how NPM1 enhances DNA binding without remaining in the complex was unknown
  22. 2018 High

    Proof that cytoplasmic NPM1c is required to maintain the AML leukemic state through HOX gene expression, and that its nuclear relocalization or degradation causes differentiation, established NPM1c localization as a therapeutic target.

    Evidence Targeted NPM1c degradation (dTAG), XPO1 inhibitor, gene expression analysis, differentiation assays, murine leukemia survival model

    PMID:30205049

    Open questions at the time
    • The mechanism by which cytoplasmic NPM1c maintains HOX expression was not yet defined
    • Whether all NPM1-mutant AML subtypes respond equivalently to relocalization was unknown
  23. 2021 High

    Identification of the ATR→SIRT7→NPM1 deacetylation→MDM2 binding cascade as the mechanism stabilizing p53 after UV damage resolved how NPM1 translocation is coupled to p53 activation via a defined enzymatic pathway.

    Evidence In vitro deacetylation assay, ATR inhibitor, co-immunoprecipitation (NPM1–MDM2), p53 ubiquitination assay, SIRT7 KO cells and mice

    PMID:33495326

    Open questions at the time
    • Which specific acetyl-lysine residue(s) on NPM1 are deacetylated by SIRT7 were not mapped
    • Whether this pathway operates for non-UV genotoxic stresses was not tested
  24. 2023 High

    Concurrent genome-wide studies demonstrating that NPM1c directly binds chromatin at HOXA/B-MEIS1 loci in cooperation with MLL1, sustains active transcription by inhibiting HDACs, and that this neomorphic function is absent from wild-type NPM1, defined the mechanistic basis for the NPM1c oncogenic transcriptional program and explained Menin inhibitor efficacy.

    Evidence ChIP-seq, CUT&RUN, ATAC-seq, RNA-seq, acute NPM1c dTAG degradation, HDAC activity assay, co-immunoprecipitation

    PMID:36455589 PMID:36455613

    Open questions at the time
    • Whether NPM1c directly contacts DNA or is recruited solely through MLL1/Menin was not resolved
    • How HDAC inhibition by NPM1c is mechanistically achieved was not defined
  25. 2024 High

    Discovery that NPM1 recruits the histone demethylase KDM5b to repress the Tsc1 promoter, thereby activating mTOR-dependent inflammatory glycolysis in cardiac macrophages, extended NPM1's chromatin-regulatory functions to metabolic and inflammatory programming beyond cancer.

    Evidence Macrophage-specific NPM1 conditional KO mice, ChIP-qPCR, RNA-seq, metabolite profiling, co-immunoprecipitation

    PMID:38390737

    Open questions at the time
    • Whether this KDM5b recruitment mechanism operates in other tissue macrophages or cell types was not tested
    • How NPM1 oligomerization state influences KDM5b recruitment was not addressed
  26. 2024 High

    Demonstration that NPM1 sequesters IRF1 from MHC-I/II gene promoters to suppress antigen presentation and promote tumor immune evasion revealed a previously unappreciated immunomodulatory function.

    Evidence Co-immunoprecipitation (NPM1–IRF1), ChIP-qPCR, dual-luciferase reporter, Npm1-KO tumors in syngeneic mice with CyTOF

    PMID:39402629

    Open questions at the time
    • Whether NPM1–IRF1 interaction is direct or mediated by a bridging factor was not fully resolved
    • Relevance to human tumors beyond the murine models used was not established

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: the structural basis for how NPM1 oligomerization, post-translational modifications, and chaperone activity are coordinately regulated; which specific acetyl-lysine sites mediate SIRT7-dependent translocation; whether NPM1c directly contacts DNA or is exclusively recruited via protein–protein interactions; and how NPM1's diverse chromatin-regulatory functions (KDM5b recruitment, HDAC inhibition, IRF1 sequestration) are integrated in different cell types.
  • No high-resolution structure of full-length NPM1 in complex with chromatin or ARF
  • Comprehensive mapping of acetylation/deacetylation sites regulating translocation is lacking
  • Integrated model connecting NPM1 chaperone, ribonuclease, and chromatin functions is absent

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 5 GO:0140110 transcription regulator activity 4 GO:0044183 protein folding chaperone 2 GO:0042393 histone binding 1 GO:0140098 catalytic activity, acting on RNA 1
Localization
GO:0005730 nucleolus 6 GO:0005815 microtubule organizing center 5 GO:0005654 nucleoplasm 4 GO:0005694 chromosome 3 GO:0005829 cytosol 2
Pathway
R-HSA-1640170 Cell Cycle 6 R-HSA-1643685 Disease 5 R-HSA-74160 Gene expression (Transcription) 5 R-HSA-162582 Signal Transduction 4 R-HSA-5357801 Programmed Cell Death 4 R-HSA-8953854 Metabolism of RNA 4 R-HSA-392499 Metabolism of proteins 3 R-HSA-4839726 Chromatin organization 3
Partners
ARFIRF1KDM5BMDM2PLK1RELAROCK2SIRT7
Complex memberships
NPM-ALK fusion oncoproteinNPM1-ARF complexNPM1c-MLL1-Menin complex

Evidence

Reading pass · 34 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2004 ARF (p14/p19) physically interacts with NPM1/B23 through the ARF amino terminus (also required for Mdm2 binding) and the central acidic domain plus oligomerization segment of NPM1. A significant proportion of ARF associates with NPM1 in high-molecular-weight complexes (2–5 MDa), and this interaction is required for ARF to retard rRNA processing; an NPM1 C-terminal deletion mutant that oligomerizes with endogenous NPM1 blocks ARF from entering these complexes and overrides ARF-dependent inhibition of rRNA processing. Tandem-affinity purification, co-immunoprecipitation, sucrose gradient sedimentation, dominant-negative NPM mutant expression in NIH 3T3 and MEF cells lacking Mdm2/p53 Molecular and cellular biology High 14729947
2004 ARF upregulation causes nucleolar retention (sequestration) of NPM1/B23 and concomitant cell cycle arrest in a p53-independent manner. Mdm2 outcompetes NPM1 for ARF binding: in vitro Mdm2 releases NPM1 from ARF-containing complexes, and in vivo Mdm2 introduction reverses ARF-mediated S-phase block without altering NPM1 protein levels, indicating that ARF's p53-independent tumor suppressor function involves blocking NPM1 nucleocytoplasmic shuttling. Inducible ARF expression system, co-immunoprecipitation, cell cycle analysis, in vitro competition assay Molecular and cellular biology High 15485902
1999 NPM1/B23 possesses molecular chaperone activity: it inhibits aggregation of denatured substrates (HIV Rev, LADH, carboxypeptidase A, citrate synthase, rhodanese) in a concentration-dependent, saturable manner, protects enzyme activity during thermal denaturation, promotes refolding of guanidine-HCl-denatured LADH, and preferentially binds denatured proteins by exposing hydrophobic regions. Turbidity/light-scattering aggregation assay, enzyme activity protection assay, refolding assay, hydrophobic-surface binding Protein science High 10211837
1995 NPM1/B23 has intrinsic ribonuclease activity demonstrated with purified recombinant B23.1 and B23.2 isoforms and natural protein, with B23.1 showing ~5-fold higher specific activity than B23.2. Activity is pH-optimum 7.5, stimulated by low Ca2+/Mg2+/NaCl, inhibited by calf thymus DNA, and insensitive to human placental RNase inhibitor, consistent with a role in preribosomal RNA processing. RNA-embedded gel assay, perchloric acid precipitation assay with bacterially expressed recombinant proteins Nucleic acids research High 7479045
1996 NPM1/B23 interacts with nucleolin (C23) and nucleolar protein p120 through specific binding domains: a ~46-amino-acid domain in B23 (residues 194–239) binds the C-terminal region of C23 (residues 540–628, required for nucleolar localization); the same B23 domain also binds a p120 fragment containing a functional nucleolar localization signal, suggesting NPM1/B23 acts as a nucleolar-localization-signal-binding protein. Yeast two-hybrid, co-immunoprecipitation from HeLa nuclear extract, deletion-mutant binding studies European journal of biochemistry High 8620867
2005 PARP-1 and PARP-2 both interact with NPM1/B23 through their N-terminal DNA-binding domains. The interaction is constitutive, independent of PARP enzymatic activity or ribosomal transcription, but is abrogated by mutation of the PARP-2 nucleolar localization signal. All three proteins co-delocalize from the nucleolus upon RNA polymerase I inhibition. Co-immunoprecipitation, colocalization by immunofluorescence, nucleolar localization signal mutation, RNA Pol I inhibition Journal of cell science High 15615785
2004 DNA damage disrupts the ARF–NPM1/B23 interaction in human tumor cells, triggering a transient p53-independent translocation of ARF from the nucleolus to the nucleoplasm, where ARF-Hdm2 complexes appear. This redistribution also unmasks the ARF C-terminus and masks its N-terminus. The pre-damage ARF–NPM1 complexes and localization patterns are restored within 24 hours after DNA repair. Immunofluorescence, co-immunoprecipitation, time-course after UV/gamma irradiation in human tumor cells Cancer research High 16267006
2006 ROCK II kinase localizes to centrosomes, physically interacts with NPM1/B23, and is an effector downstream of the CDK2/cyclin E–NPM1 pathway in centrosome duplication. ROCK II kinase activity is enhanced by binding to NPM1, and NPM1 acquires higher affinity for ROCK II upon CDK2-mediated Thr199 phosphorylation. Constitutively active ROCK II promotes centrosome duplication; ROCK II knockdown delays it. Co-immunoprecipitation, kinase activity assay, siRNA knockdown, constitutively active/dominant-negative constructs, centrosome counting Molecular and cellular biology High 17015463
2004 Polo-like kinase 1 (Plk1) phosphorylates NPM1/B23 at Ser4 specifically during mitosis. A kinase-dead Plk1 (K82M) abrogates Ser4 phosphorylation; constitutively active Plk1 (T210D) enhances it; Plk1 RNAi abolishes it. Plk1 and B23 co-immunoprecipitate and interact in GST pull-down. Interference with Ser4 phosphorylation (S4A mutant) causes aberrant centrosome numbers, nuclear elongation/fragmentation, and incomplete cytokinesis. In vivo and in vitro kinase assay, Plk1 mutants (kinase-dead, constitutively active), RNAi, co-immunoprecipitation, GST pull-down, phenotypic analysis The Journal of biological chemistry High 15190079
2010 Polo-like kinase 2 (Plk2) phosphorylates NPM1/B23 at Ser4 in S-phase. Plk2 and NPM1 interact in vitro in a Polo-box-dependent manner and co-immunoprecipitate in vivo. A non-phosphorylatable S4A mutant of NPM1 interferes with centriole reduplication in S-phase-arrested cells and leads to centriole dilution in cycling cells; the phosphomimetic S4D mutant causes centriole accumulation. In vitro kinase assay, Polo-box domain interaction assay, co-immunoprecipitation, S4A/S4D mutant expression, centriole counting PloS one High 20352051
2007 NPM1/B23 is sumoylated primarily at Lys263 (and secondarily at Lys230). K263 sumoylation is required for NPM1 centrosomal and nucleolar residency. Rb binds wild-type NPM1 but not the K263R mutant; sumoylation enhances NPM1–Rb interaction, and NPM1 potently stimulates E2F1-mediated transcriptional activity (abolished by K263R). K263R also renders NPM1 vulnerable to caspase-3 cleavage, sensitizing cells to apoptosis. K230R strongly binds phosphatidylinositol-3,4,5-trisphosphate and suppresses DNA fragmentation. Sumoylation assay, site-directed mutagenesis, co-immunoprecipitation (Rb), transcriptional reporter assay (E2F1), caspase-3 cleavage assay, PI(3,4,5)P3 binding assay Proceedings of the National Academy of Sciences of the United States of America High 17535915
2021 SIRT7 deacetylates NPM1 in response to UV irradiation. ATR-mediated phosphorylation of SIRT7 increases its catalytic activity, promoting NPM1 deacetylation. Deacetylated NPM1 translocates from the nucleolus to the nucleoplasm and binds MDM2, preventing ubiquitination and degradation of p53, thereby enabling cell-cycle arrest and DNA repair. In SIRT7-deficient cells, UV-induced p53 stabilization is abrogated both in vitro and in vivo. In vitro deacetylation assay, ATR inhibitor/kinase assay, co-immunoprecipitation (NPM1–MDM2), p53 ubiquitination assay, SIRT7 KO cells and mice, UV-irradiation time-course Proceedings of the National Academy of Sciences of the United States of America High 33495326
2017 NPM1 directly associates with the DNA-binding domain of NF-κB p65 and enhances p65 DNA-binding activity through a chaperone-like function, without itself becoming part of the DNA–NF-κB complex. NPM1 knockdown reduces NF-κB-mediated transcription, decreases p65 recruitment to target gene promoters, and impairs inflammatory gene expression (TNF-α, LPS stimulation) and NF-κB-dependent invasion of breast cancer cells. Co-immunoprecipitation, ChIP, siRNA knockdown, luciferase reporter assay, invasion assay Nucleic acids research High 28003476
2009 NPM1/B23 directly binds p21WAF1/CIP1, confirmed by reciprocal co-immunoprecipitation and GST pull-down. NPM1 overexpression prolongs p21 half-life and inhibits p21 ubiquitination; NPM1 knockdown destabilizes p21 and increases its ubiquitination. Co-localization of NPM1 and p21 in the nucleoplasm increases upon actinomycin D-induced NPM1 translocation. Reciprocal co-immunoprecipitation, GST pull-down, confocal microscopy, pulse-chase half-life assay, ubiquitination assay, siRNA knockdown Cell cycle High 19221506
2018 Mutant NPM1 (NPM1c) is required to maintain the leukemic state through sustained HOX gene expression. Loss of NPM1c from the cytoplasm—either by nuclear relocalization or targeted degradation—causes immediate downregulation of HOX genes followed by AML cell differentiation. XPO1 inhibition relocalizes NPM1c to the nucleus, promotes differentiation of AML cells, and prolongs survival in Npm1-mutated leukemic mice. Targeted protein degradation (dTAG), XPO1 inhibitor treatment, gene expression analysis, differentiation assays, murine leukemia model survival Cancer cell High 30205049
2023 NPM1c directly binds to specific chromatin targets co-occupied by the histone methyltransferase KMT2A (MLL1). Targeted degradation of NPM1c leads to rapid decrease in gene expression, loss of RNA Pol II, and loss of activating histone modifications at target loci (including HOXA/B cluster and MEIS1). NPM1c functions as a direct transcriptional regulator in collaboration with the MLL1 complex, providing the mechanism by which MLL1-Menin inhibitors produce clinical responses. ChIP-seq, CUT&RUN, targeted NPM1c degradation (dTAG), RNA-seq, co-immunoprecipitation Cancer discovery High 36455613
2023 NPM1c binds to a subset of active gene promoters in NPM1c AML cells (including HOXA/B and MEIS1), sustains active transcription by orchestrating a transcription hub, and maintains active chromatin by inhibiting histone deacetylases. This neomorphic chromatin-binding function of NPM1c is absent from wild-type NPM1. ChIP-seq, ATAC-seq, RNA-seq, HDAC activity assay, co-immunoprecipitation Cancer discovery High 36455589
2008 Npm1 acts as a haploinsufficient tumor suppressor in the hematopoietic compartment. Npm1+/- mice display greater propensity for myeloid and lymphoid malignancies compared with wild-type littermates. Malignant cells retain the wild-type allele with normal NPM1 localization and expression, showing that complete Npm1 loss is not required for tumorigenesis. Npm1 heterozygous knockout mouse model, longitudinal tumor surveillance, immunohistochemistry, Western blot Blood High 18212245
1997 NPM-ALK fusion protein, generated by t(2;5), is sufficient to cause B-lineage large-cell lymphoma in mice when expressed via retroviral gene transfer into bone marrow. Tumors express NPM-ALK, are clonal with Ig heavy- and kappa-chain rearrangements, and are transplantable into secondary recipients, establishing NPM-ALK as a direct causative oncogene. Retroviral gene transfer, bone marrow transplantation, immunoblot, immunohistochemistry, Southern blot for clonality, secondary transplantation Blood High 9376569
2014 Aurora kinases A and B phosphorylate NPM1 at Ser125 in vitro and in vivo. Phospho-S125-NPM1 localizes to the midbody during late cytokinesis, co-localizing with Aurora B. Overexpression of a non-phosphorylatable S125A mutant causes deregulated centrosome duplication, elongated/fragmented nuclei, and cytokinesis failure. In vitro kinase assay, phospho-specific antibody, immunofluorescence localization, S125A mutant overexpression with mitotic phenotype analysis FEBS letters High 24857377
2007 Ebp1 isoforms p42 and p48 form complexes with NPM1/B23 with differential requirements. p48 constitutively binds NPM1 in the nucleolus, requiring NPM1 Lys263 sumoylation. p42 selectively binds unsumoylated NPM1 upon EGF stimulation, requiring Ser360 phosphorylation of p42. The NPM1–Ebp1 complex regulates ribosome biogenesis and cell survival; knockdown of either reduces ribosomal output and viability. Co-immunoprecipitation, sumoylation-deficient NPM1 mutants, phospho-mutant p42, siRNA knockdown, ribosome biogenesis assay, viability assay The Journal of biological chemistry High 17951246
2015 CD24 competitively inhibits ARF binding to NPM1, resulting in decreased ARF levels, increased MDM2, and decreased p53 and p21/CDKN1A. CD24 silencing prevents functional inactivation of p53 by somatic mutation and viral oncogenes (SV40 large T, HPV16 E6). Co-immunoprecipitation competition assay, shRNA/targeted mutation of CD24, Western blot for ARF/MDM2/p53/p21, rescue experiments Nature communications High 25600590
2014 AKT phosphorylation of NPM at Ser48 prevents NPM oligomerization, resulting in nucleoplasmic localization of ARF and constitutive MDM2 inhibition, thereby stabilizing p53. Oligomeric NPM drives nucleolar accumulation of ARF; formation of NPM/ARF oligomers antagonizes MDM2 E3-ligase inhibitory complex, activating MDM2 toward p53. AKT/PI3K inhibitors promote ARF nucleolar localization and reduce mutant p53 stability in vivo. Co-immunoprecipitation, AKT kinase assay, NPM oligomerization assay, phospho-S48 NPM analysis, xenograft model with AKT inhibitor MK-2206 Oncotarget Medium 25071014
1992 NPM1/B23 nucleolar-to-nucleoplasm translocation (B23-translocation) induced by cytotoxic drugs (camptothecin, actinomycin D) is a reversible redistribution process: upon removal of camptothecin, NPM1 relocalizes to nucleoli within 2 h in the presence of cycloheximide, indicating redistribution of existing protein without new synthesis. Phosphorylation status and oligomeric state of NPM1 do not change during drug-induced translocation. Drug washout experiments with cycloheximide, immunolocalization, cross-linking/gel electrophoresis for oligomeric state, 32P phosphorylation analysis Experimental cell research Medium 1426041
2024 Oligomeric NPM1 recruits histone demethylase KDM5b to the Tsc1 promoter, reducing H3K4me3 modification and inhibiting TSC1 expression, which facilitates mTOR-dependent inflammatory glycolysis in cardiac macrophages and antagonizes their reparative function after myocardial infarction. Macrophage-specific NPM1 deletion shifts metabolism from glycolysis to oxidative phosphorylation. Macrophage-specific NPM1 KO mice, ChIP-qPCR, RNA-seq, metabolite profiling, Co-IP (NPM1–KDM5b), H3K4me3 ChIP Circulation High 38390737
2024 NPM1 associates with transcription factor IRF1 and sequesters IRF1 from binding to the Nlrc5 and Ciita promoters, suppressing IRF1-mediated transcription of MHC-I and MHC-II molecules in tumor cells, thereby promoting immune evasion. NPM1 loss increases MHC-I/II expression and enhances CD8+ T-cell-mediated killing. Co-immunoprecipitation (NPM1–IRF1), dual-luciferase reporter assay, ChIP-qPCR (IRF1 binding at Nlrc5/Ciita), Npm1-KO tumor cells in syngeneic mice, flow cytometry, CyTOF Journal of hematology & oncology High 39402629
2016 In ALK-rearranged ALCL cells, only cytoplasmic NPM-ALK is catalytically active; nuclear NPM-ALK is inactive due to heterodimerization with endogenous NPM1. About 50% of NPM-ALK is sequestered as inactive NPM-ALK/NPM1 heterodimers in the nucleus. Overexpression or cytoplasmic relocalization of NPM-ALK (by NPM1 knockout) causes ERK1/2 hyperphosphorylation and apoptosis via ATM/Chk2- and γH2AX-mediated DNA-damage response. Nuclear/cytoplasmic fractionation, kinase activity assay, NPM1 siRNA/KO, co-immunoprecipitation, ERK1/2 phosphorylation, γH2AX detection Oncogene High 26657151
2011 NPM-ALK regulates phosphorylation of GSK3β at Ser9 via the PI3K/AKT signaling pathway, inhibiting GSK3β activity and thereby stabilizing its substrates Mcl-1 and CDC25A. ALK inhibition leads to GSK3β-dependent proteasomal degradation of Mcl-1 and CDC25A; GSK3β inhibition rescues viability upon ALK inhibition, and GSK3β knockdown confers resistance to ALK inhibitor-induced growth arrest. Phosphoproteomic mass spectrometry screen, ALK kinase inhibitor, K210R kinase-dead NPM-ALK mutant, GSK3β siRNA/inhibitor, proteasome inhibitor rescue Oncogene High 22179823
2009 NPM-ALK inhibits the p53 tumor suppressor pathway through MDM2 upregulation and JNK-dependent mechanisms. Constitutive ALK signaling leads to functional inactivation/degradation of p53 in JNK- and MDM2-dependent manners, and nuclear exclusion of p53 in a PI3K-dependent manner. Pharmacological inhibition of JNK, PI3K, or MDM2 reactivates p53 and induces apoptosis in ALK-expressing cells. ALK kinase inhibition, JNK/PI3K inhibitors, p53 immunofluorescence (nuclear exclusion), MDM2 inhibitor, apoptosis assay Blood High 19286999
2006 AUF1/hnRNPD is a binding partner of NPM-ALK (and other X-ALK fusions). AUF1 co-immunoprecipitates with ALK in ALCL cells and in NIH3T3 cells expressing NPM-ALK; both proteins concentrate in cytoplasmic foci requiring ALK kinase activity. AUF1 is phosphorylated by ALK in vitro and is hyperphosphorylated in NPM-ALK-expressing cells, correlating with increased stability of AUF1 target mRNAs encoding proliferation regulators and increased cell survival after transcriptional arrest. Co-immunoprecipitation, in vitro kinase assay, immunofluorescence co-localization, mRNA stability assay Blood Medium 16835382
2015 NPM1/B23 interaction with linker histone H1.5 supports glioma cell survival. NPM1 depletion sensitizes glioma cells to actinomycin D-induced apoptosis. Silencing of H1.5 triggers glioma cell apoptosis (cleaved caspase-3, cleaved PARP); enforced NPM1 expression suppresses H1.5-depletion-induced apoptosis, demonstrating that NPM1 functions downstream of or alongside H1.5 in an anti-apoptotic pathway. siRNA knockdown (NPM1, H1.5), caspase-3 cleavage, PARP cleavage, NPM1 rescue overexpression, actinomycin D treatment Scientific reports Medium 26559910
2010 NPM-ALK fusion protein induces HIF1α mRNA expression under normoxia in T-cell lymphoma cells through STAT3, which binds to the HIF1α gene promoter. This was shown by ChIP demonstrating STAT3 occupancy at the HIF1α promoter, STAT3 siRNA abolishing HIF1α expression, and kinase-inactive NPM-ALK K210R failing to induce HIF1α, whereas ALK inhibitor abolishes expression. ChIP assay (STAT3 at HIF1α promoter), siRNA (STAT3), kinase-inactive NPM-ALK K210R mutant, ALK small-molecule inhibitor, RT-PCR/Western Oncogene Medium 21102525
2016 NPM-ALK phosphorylates WASp at its canonical activation site (Y290) and at a novel residue (Y102). Y102 phosphorylation negatively regulates WASp interaction with Wiskott-Aldrich interacting protein, decreases WASp protein stability, and enhances anchorage-independent growth and tumor growth in vivo. WASp knockdown or Y102F mutation decreases colony formation and xenograft tumor growth. Phosphoproteomics, in vitro ALK kinase assay on WASp, co-immunoprecipitation, Y102F/Y290F mutants, xenograft model, colony formation assay Oncogene High 27694894
1997 NPM1/B23 undergoes cell cycle-dependent translocation: it is nucleolar at interphase, disperses to the nucleoplasm at prophase, then appears in the cytoplasm from prometaphase to mid-telophase, in the perichromosomal layer (from prometaphase to early telophase, associated with RNA), in cytoplasmic bodies at anaphase/telophase, and in prenucleolar bodies at telophase. Mitotic B23 shows slower SDS-PAGE mobility (consistent with phosphorylation). Cytoplasmic mitotic B23 is RNA-free and Triton-extractable, unlike perichromosomal B23. Immunofluorescence in three cell lines, cell extraction with Triton/RNase, Western blot mobility shift, monoclonal antibody 20B2 European journal of cell biology Medium 9174672

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2023 The menin inhibitor revumenib in KMT2A-rearranged or NPM1-mutant leukaemia. Nature 396 36922593
2004 Physical and functional interactions of the Arf tumor suppressor protein with nucleophosmin/B23. Molecular and cellular biology 328 14729947
2018 Mutant NPM1 Maintains the Leukemic State through HOX Expression. Cancer cell 262 30205049
2020 NPM1-mutated acute myeloid leukemia: from bench to bedside. Blood 261 32609823
2010 NPM1/B23: A Multifunctional Chaperone in Ribosome Biogenesis and Chromatin Remodeling. Biochemistry research international 249 21152184
1999 Nucleolar protein B23 has molecular chaperone activities. Protein science : a publication of the Protein Society 208 10211837
1997 Retrovirus-mediated gene transfer of NPM-ALK causes lymphoid malignancy in mice. Blood 208 9376569
2010 Acute myeloid leukemia with mutated nucleophosmin (NPM1): is it a distinct entity? Blood 197 21030560
2005 PARP-1 and PARP-2 interact with nucleophosmin/B23 and accumulate in transcriptionally active nucleoli. Journal of cell science 163 15615785
1999 Lymphomas expressing ALK fusion protein(s) other than NPM-ALK. Blood 155 10552961
2017 Biological and clinical consequences of NPM1 mutations in AML. Leukemia 151 28111462
1996 C23 interacts with B23, a putative nucleolar-localization-signal-binding protein. European journal of biochemistry 139 8620867
2004 ARF impedes NPM/B23 shuttling in an Mdm2-sensitive tumor suppressor pathway. Molecular and cellular biology 136 15485902
1996 Expression of nucleophosmin/B23 in normal and neoplastic colorectal mucosa. The Journal of pathology 130 8778315
1995 The ribonuclease activity of nucleolar protein B23. Nucleic acids research 125 7479045
2023 Mutant NPM1 Directly Regulates Oncogenic Transcription in Acute Myeloid Leukemia. Cancer discovery 108 36455613
2005 DNA damage disrupts the p14ARF-B23(nucleophosmin) interaction and triggers a transient subnuclear redistribution of p14ARF. Cancer research 105 16267006
2019 Clonal evolution patterns in acute myeloid leukemia with NPM1 mutation. Nature communications 104 31048683
2008 Npm1 is a haploinsufficient suppressor of myeloid and lymphoid malignancies in the mouse. Blood 100 18212245
2007 Sumoylation of nucleophosmin/B23 regulates its subcellular localization, mediating cell proliferation and survival. Proceedings of the National Academy of Sciences of the United States of America 83 17535915
2007 Increased expression of nucleophosmin/B23 in hepatocellular carcinoma and correlation with clinicopathological parameters. British journal of cancer 81 17245342
2006 Interaction between ROCK II and nucleophosmin/B23 in the regulation of centrosome duplication. Molecular and cellular biology 80 17015463
2020 CircRNA WHSC1 targets the miR-646/NPM1 pathway to promote the development of endometrial cancer. Journal of cellular and molecular medicine 79 32378344
2023 Mutant NPM1 Hijacks Transcriptional Hubs to Maintain Pathogenic Gene Programs in Acute Myeloid Leukemia. Cancer discovery 78 36455589
2017 When the good go bad: Mutant NPM1 in acute myeloid leukemia. Blood reviews 75 29157973
2004 B23/nucleophosmin serine 4 phosphorylation mediates mitotic functions of polo-like kinase 1. The Journal of biological chemistry 72 15190079
2018 NPM1 mutated AML can relapse with wild-type NPM1: persistent clonal hematopoiesis can drive relapse. Blood advances 70 30455361
1992 Characterization and cellular localization of nucleophosmin/B23 in HeLa cells treated with selected cytotoxic agents (studies of B23-translocation mechanism). Experimental cell research 66 1426041
2024 Molecular, clinical, and therapeutic determinants of outcome in NPM1-mutated AML. Blood 64 38691678
2021 How I diagnose and treat NPM1-mutated AML. Blood 63 33171486
2019 Clinicopathologic and genetic characterization of nonacute NPM1-mutated myeloid neoplasms. Blood advances 62 31085507
2012 Expression of nucleophosmin/NPM1 correlates with migration and invasiveness of colon cancer cells. Journal of biomedical science 60 22631075
2015 Intracellular CD24 disrupts the ARF-NPM interaction and enables mutational and viral oncogene-mediated p53 inactivation. Nature communications 58 25600590
2003 Nucleophosmin/B23 is a proliferate shuttle protein associated with nuclear matrix. Journal of cellular biochemistry 56 14635188
1990 Structure of the gene for rat nucleolar protein B23. The Journal of biological chemistry 55 2211699
2006 DNA damage, p14ARF, nucleophosmin (NPM/B23), and cancer. Journal of molecular histology 54 16855788
2005 Nucleophosmin/B23, a multifunctional protein that can regulate apoptosis. Cancer biology & therapy 53 16103750
2024 Targeting NPM1 Epigenetically Promotes Postinfarction Cardiac Repair by Reprogramming Reparative Macrophage Metabolism. Circulation 52 38390737
2021 The potential role of nucleophosmin (NPM1) in the development of cancer. Journal of cellular physiology 52 33959979
2015 CDApps: integrated software for experimental planning and data processing at beamline B23, Diamond Light Source. Journal of synchrotron radiation 52 25723950
2007 Ebp1 association with nucleophosmin/B23 is essential for regulating cell proliferation and suppressing apoptosis. The Journal of biological chemistry 51 17951246
1995 Nucleophosmin/B23 (NPM) oligomer is a major and stable entity in HeLa cells. Biochimica et biophysica acta 51 7772597
2021 SIRT7-dependent deacetylation of NPM promotes p53 stabilization following UV-induced genotoxic stress. Proceedings of the National Academy of Sciences of the United States of America 50 33495326
2017 Efficient DNA binding of NF-κB requires the chaperone-like function of NPM1. Nucleic acids research 49 28003476
2015 IDH2 and NPM1 Mutations Cooperate to Activate Hoxa9/Meis1 and Hypoxia Pathways in Acute Myeloid Leukemia. Cancer research 49 25795706
2017 Coexisting and cooperating mutations in NPM1-mutated acute myeloid leukemia. Leukemia research 48 28152414
2006 A "liaison dangereuse" between AUF1/hnRNPD and the oncogenic tyrosine kinase NPM-ALK. Blood 45 16835382
1997 Cell cycle-dependent translocations of a major nucleolar phosphoprotein, B23, and some characteristics of its variants. European journal of cell biology 44 9174672
2015 Chronic myelomonocytic leukemia with nucleophosmin (NPM1) mutation. European journal of haematology 43 25809997
2015 NPM1 histone chaperone is upregulated in glioblastoma to promote cell survival and maintain nucleolar shape. Scientific reports 42 26559910
2006 B23 and ARF: friends or foes? Cell biochemistry and biophysics 42 16943625
2005 What have we learnt from mouse models of NPM-ALK-induced lymphomagenesis? Leukemia 41 15902287
1996 PML, PLZF and NPM genes in the molecular pathogenesis of acute promyelocytic leukemia. Haematologica 41 8952164
2015 Excess of NPM-ALK oncogenic signaling promotes cellular apoptosis and drug dependency. Oncogene 39 26657151
2022 Targeted therapy in NPM1-mutated AML: Knowns and unknowns. Frontiers in oncology 38 36237321
1995 Detection of NPM-ALK DNA rearrangement in CD30 positive anaplastic large cell lymphoma. British journal of haematology 37 7772531
2009 NPM-ALK inhibits the p53 tumor suppressor pathway in an MDM2 and JNK-dependent manner. Blood 36 19286999
2021 Significance of NPM1 Gene Mutations in AML. International journal of molecular sciences 35 34576201
2020 IL10RA modulates crizotinib sensitivity in NPM1-ALK+ anaplastic large cell lymphoma. Blood 35 32573700
2021 Biological and therapeutic implications of a unique subtype of NPM1 mutated AML. Nature communications 34 33594052
2015 Reversal of microRNA-150 silencing disadvantages crizotinib-resistant NPM-ALK(+) cell growth. The Journal of clinical investigation 34 26258416
2011 Autoregulatory circuit of human rpL3 expression requires hnRNP H1, NPM and KHSRP. Nucleic acids research 34 21705779
2010 Polo-like kinase 2-dependent phosphorylation of NPM/B23 on serine 4 triggers centriole duplication. PloS one 34 20352051
2007 Oncogenic role of nucleophosmin/B23. Chang Gung medical journal 34 17939258
2018 Inactivation of PBX3 and HOXA9 by down-regulating H3K79 methylation represses NPM1-mutated leukemic cell survival. Theranostics 33 30214626
2020 Nucleophosmin1 (NPM1) abnormality in hematologic malignancies, and therapeutic targeting of mutant NPM1 in acute myeloid leukemia. Therapeutic advances in hematology 32 32071709
2009 Nucleophosmin/B23 interacts with p21WAF1/CIP1 and contributes to its stability. Cell cycle (Georgetown, Tex.) 32 19221506
2007 Role of Npm1 in proliferation, apoptosis and differentiation of neural stem cells. Journal of the neurological sciences 32 17949752
2021 CD123 Is Consistently Expressed on NPM1-Mutated AML Cells. Cancers 31 33525388
2004 The ARF-B23 connection: implications for growth control and cancer treatment. Cell cycle (Georgetown, Tex.) 31 14726681
2014 AKT regulates NPM dependent ARF localization and p53mut stability in tumors. Oncotarget 30 25071014
2013 The human NPM1 mutation A perturbs megakaryopoiesis in a conditional mouse model. Blood 30 23435463
2010 Oncogenic kinase NPM/ALK induces expression of HIF1α mRNA. Oncogene 30 21102525
2025 Azacitidine, Venetoclax, and Revumenib for Newly Diagnosed NPM1-Mutated or KMT2A-Rearranged AML. Journal of clinical oncology : official journal of the American Society of Clinical Oncology 29 40504618
2024 Criteria for Diagnosis and Molecular Monitoring of NPM1-Mutated AML. Blood cancer discovery 29 37917833
2011 NPM-ALK signals through glycogen synthase kinase 3β to promote oncogenesis. Oncogene 29 22179823
2006 Loss of the NPM1 gene in myeloid disorders with chromosome 5 rearrangements. Leukemia 28 16341035
2019 LncRNA SAMD12-AS1 promotes cell proliferation and inhibits apoptosis by interacting with NPM1. Scientific reports 27 31406141
2014 miR-21 is overexpressed in NPM1-mutant acute myeloid leukemias. Leukemia research 27 25543261
2016 Redundant and nonredundant roles for Cdc42 and Rac1 in lymphomas developed in NPM-ALK transgenic mice. Blood 26 26747246
2016 Phosphorylated STAT5 regulates p53 expression via BRCA1/BARD1-NPM1 and MDM2. Cell death & disease 26 28005077
2013 NPM-ALK up-regulates iNOS expression through a STAT3/microRNA-26a-dependent mechanism. The Journal of pathology 25 23338972
2020 Nucleolar protein NPM1 is essential for circovirus replication by binding to viral capsid. Virulence 23 33073687
2024 NPM1 inhibits tumoral antigen presentation to promote immune evasion and tumor progression. Journal of hematology & oncology 22 39402629
2019 MYCT1 represses apoptosis of laryngeal cancerous cells through the MAX/miR-181a/NPM1 pathway. The FEBS journal 22 31152622
2023 Cytoplasmic Expression of TP53INP2 Modulated by Demethylase FTO and Mutant NPM1 Promotes Autophagy in Leukemia Cells. International journal of molecular sciences 21 36675134
2012 Estrogen stimulates the proliferation of human endometrial cancer cells by stabilizing nucleophosmin/B23 (NPM/B23). Journal of molecular medicine (Berlin, Germany) 21 22926011
2024 Functions of the native NPM1 protein and its leukemic mutant. Leukemia 20 39690184
2018 INPP4B promotes cell survival via SGK3 activation in NPM1-mutated leukemia. Journal of experimental & clinical cancer research : CR 20 29343273
2014 Phosphorylation of multifunctional nucleolar protein nucleophosmin (NPM1) by aurora kinase B is critical for mitotic progression. FEBS letters 20 24857377
2012 A knock-in Npm1 mutation in mice results in myeloproliferation and implies a perturbation in hematopoietic microenvironment. PloS one 20 23226219
2024 AURKA inhibition induces Ewing's sarcoma apoptosis and ferroptosis through NPM1/YAP1 axis. Cell death & disease 19 38287009
2021 NPM-ALK: A Driver of Lymphoma Pathogenesis and a Therapeutic Target. Cancers 19 33466277
2016 NPM-ALK phosphorylates WASp Y102 and contributes to oncogenesis of anaplastic large cell lymphoma. Oncogene 19 27694894
2015 Insights into the regulation of neuronal viability by nucleophosmin/B23. Experimental biology and medicine (Maywood, N.J.) 19 25908633
2010 Akt2 and nucleophosmin/B23 function as an oncogenic unit in human lung cancer cells. Experimental cell research 19 21182834
2019 Implication of B23/NPM1 in Viral Infections, Potential Uses of B23/NPM1 Inhibitors as Antiviral Therapy. Infectious disorders drug targets 18 29589547
2022 Neutrophil extracellular traps arm DC vaccination against NPM-mutant myeloproliferation. eLife 16 35471185
2017 Nucleophosmin (NPM1)/B23 in the Proteome of Human Astrocytic Cells Restricts Chikungunya Virus Replication. Journal of proteome research 16 28959884
2015 Involvement of Nucleophosmin (NPM1/B23) in Assembly of Infectious HPV16 Capsids. Papillomavirus research (Amsterdam, Netherlands) 16 27398412