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Showing KDM2B — FBXL10 is a alias.

KDM2B

Lysine-specific demethylase 2B · UniProt Q8NHM5

Length
1336 aa
Mass
152.6 kDa
Annotated
2026-06-10
100 papers in source corpus 46 papers cited in narrative 46 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/8 claims corpus-supported (88%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

KDM2B (FBXL10/JHDM1b) is a multi-domain chromatin regulator that links sequence-specific recognition of CpG island DNA to Polycomb-mediated gene silencing, and that also possesses Jumonji-domain histone demethylase and F-box-dependent ubiquitin-ligase activities (PMID:23256043, PMID:18836456, PMID:26725323). Its defining activity is recognition of non-methylated CpG islands through the CxxC zinc-finger domain, which recruits a noncanonical PRC1 complex (PRC1.1 containing RING1B/RNF2, PCGF1/NSPC1, BCOR/BCORL1, SKP1) to catalyze H2AK119 monoubiquitylation and repress target genes genome-wide (PMID:23256043, PMID:23395003, PMID:23502314, PMID:17296600); the BCORL1 PUFD–PCGF1 RAWUL interface defines an architecture unique to PRC1.1 and explains how KDM2B engages both PRC1.1 and an SCF ubiquitin ligase (PMID:27568929). Both DNA binding and PRC1 integration are required for H2AK119ub1, and KDM2B loss collapses RING1B chromatin occupancy (PMID:23395003). Through this PRC1.1 axis KDM2B maintains the undifferentiated ESC state, drives somatic reprogramming, protects Polycomb-bound promoters from aberrant de novo DNA methylation, and restrains lineage- and signaling-specific gene programs including NOTCH1 and Wnt targets (PMID:23502314, PMID:25848754, PMID:29166607, PMID:31471323, PMID:37838801). Independently, the JmjC domain demethylates H3K36me1/2 — silencing the p15(Ink4b) and Ink4a/Arf loci to control senescence, proliferation, and leukemic transformation — and removes H3K4me3 at rDNA to repress rRNA transcription in the nucleolus (PMID:18836456, PMID:17994099, PMID:21310926, PMID:19202064); reported additional substrates include H3K79me2/3 and the non-histone protein SRF (PMID:29763382, PMID:33564100). As an F-box subunit, KDM2B assembles an SCF E3 ligase that polyubiquitylates c-Fos for degradation (PMID:26725323). KDM2B sustains EZH2 expression by demethylating H3K36me2 at tumor-suppressor miRNA loci (let-7, miR-101) (PMID:21757686, PMID:33091189), and is recruited to DNA damage sites via PARP1/TIMELESS to promote H2A.Z loading and homologous recombination (PMID:29985131). Loss or CxxC-domain variants of KDM2B cause neurodevelopmental syndromes via failed PRC1 recruitment and Wnt de-repression (PMID:37838801, PMID:35128353, PMID:40420380).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 2007 Medium

    Established the first functional activities of KDM2B: nucleolar repression of rRNA transcription via JmjC-dependent H3K4me3 demethylation, and tethering of repressor complexes to unmethylated CpG DNA via the CxxC zinc finger, framing it as a chromatin-targeted repressor.

    Evidence Nucleolar localization with rDNA ChIP and in vitro demethylase assay; Co-IP/ChIP at the c-jun promoter with CxxC DNA-binding assay; MS purification of a Ring1B complex containing KDM2B

    PMID:17296600 PMID:17704768 PMID:17994099

    Open questions at the time
    • H3K4me3 substrate assignment later contested by H3K36 demethylase findings
    • noncanonical Ring1B complex composition defined biochemically but not reconstituted
  2. 2008 High

    Defined KDM2B's core enzymatic identity as an H3K36 demethylase and connected it to senescence control, showing it represses p15(Ink4b) in an activity-dependent manner.

    Evidence In vitro demethylase assay, ChIP, shRNA knockdown with genetic p15 rescue in MEFs

    PMID:18836456

    Open questions at the time
    • mechanism linking H3K36 demethylation to recruitment of repressive machinery not resolved
    • does not address CpG-island/PRC1 function
  3. 2009 Medium

    Linked KDM2B to the broader Polycomb network, showing it counteracts senescence-associated EZH2 loss and promotes H3K27me3 and BMI1 binding at Ink4a/Arf, positioning it upstream of PRC2/PRC1 output.

    Evidence ChIP, KDM2B–EZH2 Co-IP, shRNA knockdown and histone-modification analysis in MEFs

    PMID:19202064

    Open questions at the time
    • direct vs indirect basis of EZH2 cooperation unresolved
    • single lab
  4. 2011 Medium

    Showed KDM2B sustains EZH2 by silencing EZH2-targeting tumor-suppressor miRNAs through locus-specific H3K36me2 demethylation, and established its requirement for leukemic transformation.

    Evidence ChIP, shRNA, miRNA gain/loss epistasis in MEFs; retroviral transformation and in vivo leukemia models with H3K36me2 demethylase assay; FGF2–DYRK1A–CREB induction with reporter assays

    PMID:21310926 PMID:21757686 PMID:21777817

    Open questions at the time
    • feedback-loop kinetics in primary tissue not addressed
    • miRNA-locus demethylation shown by ChIP but not directly causally separated from PRC1 effects
  5. 2012 High

    Resolved the central CpG-island-targeting model: KDM2B binds unmethylated CGIs genome-wide via CxxC and recruits PRC1 to deposit H2AK119ub1, providing a sampling mechanism for Polycomb silencing, and enables iPSC reprogramming.

    Evidence Genome-wide ChIP-seq, Co-IP, domain mutagenesis in mouse ESCs; reprogramming assays with demethylase/DNA-binding mutants

    PMID:22522173 PMID:22825849 PMID:23256043

    Open questions at the time
    • conflicting in vitro substrate assignment (H3K4me3 vs H3K36me2) in one study
    • how low-occupancy sampling is converted to stable repression unclear
  6. 2013 High

    Defined the noncanonical PRC1.1 requirement, showing both DNA binding and PRC1 integration are needed for H2AK119ub1 and RING1B recruitment, and that this axis maintains the ESC undifferentiated state and drives cancer gene programs.

    Evidence Co-IP, genome-wide ChIP-seq, domain-mutant rescue in mESCs; ChIP-seq and gain/loss-of-function in PDAC model

    PMID:23321669 PMID:23395003 PMID:23502314

    Open questions at the time
    • dual repressive (Polycomb) and activating (MYC/KDM5A) programs mechanistically distinct but switch undefined
    • stoichiometry of KDM2B within PRC1.1 in vivo unresolved
  7. 2015 High

    Demonstrated a protective genomic function: KDM2B shields Polycomb-occupied CpG-island promoters from de novo DNA methylation, with loss causing midgestation lethality not phenocopied by PRC mutants.

    Evidence Complete and conditional mouse knockout with whole-genome bisulfite sequencing and ChIP; HSC overexpression transgenic leukemia model

    PMID:25848754 PMID:25872778

    Open questions at the time
    • molecular basis for excluding DNMTs from CGIs not defined
    • relationship between methylation protection and H2AK119ub1 deposition unresolved
  8. 2016 High

    Established KDM2B's second catalytic identity as an F-box SCF E3 ligase subunit targeting c-Fos, and solved the structure explaining how it bridges PRC1.1 and SCF, while extending PRC1.1 recruitment to non-stem contexts.

    Evidence Crystal structure of KDM2B/SKP1/BCORL1/PCGF1; in vitro ubiquitylation assay and S374 mutagenesis for c-Fos; ChIP-seq/domain analysis in adipogenesis; KO mouse hematopoietic studies

    PMID:25533466 PMID:26725323 PMID:26808549 PMID:27568929

    Open questions at the time
    • full substrate repertoire of SCF^KDM2B beyond c-Fos unknown
    • regulation of switching between PRC1.1 and SCF assembly in cells undefined
  9. 2018 High

    Connected KDM2B to genome maintenance and expanded its substrate scope, showing PARP1/TIMELESS-dependent recruitment to DNA damage sites for H2A.Z loading and HR, and reporting H3K79 demethylase activity.

    Evidence Live-cell recruitment imaging, ChIP, HR assays for FRRUC; in vitro H3K79 demethylase assay with genome-wide validation; Co-IP/ChIP for EBNA3C interaction

    PMID:29502955 PMID:29763382 PMID:29985131 PMID:30135119

    Open questions at the time
    • H3K79 demethylase activity is a novel substrate claim needing independent replication
    • how FRRUC composition relates to PRC1.1 at undamaged chromatin unclear
  10. 2020 Medium

    Extended KDM2B mechanisms to S-phase control and demethylase-independent gene regulation, showing H3K79 demethylation governs PCNA dissociation and that DNA-binding (not catalysis) drives EMT and Wnt repression.

    Evidence iPOND, ITC, DNA fiber assays in 293T cells; ChIP/domain mutants for EMT and TGF-β; isoform Co-IP with TCF7L1

    PMID:33029857 PMID:33091189 PMID:33104714 PMID:33779563

    Open questions at the time
    • replication-timing role depends on contested H3K79 activity
    • demethylase-independent functions mechanistically attributed to PRC1 recruitment but not fully separated
  11. 2021 Medium

    Identified non-histone and stabilization-based functions, including SRF K165 demethylation balanced by SET7, ERRα and SNAI1 stabilization, and Brg1-dependent IL-6 induction.

    Evidence In vitro demethylase assay on SRF, Co-IP, ChIP, ubiquitylation assays, KO mouse phenotypes

    PMID:31197256 PMID:33450359 PMID:33564100 PMID:34718323

    Open questions at the time
    • non-histone substrate generality unknown
    • how a single protein partitions among demethylase, ligase, and scaffold roles in a given cell undefined
  12. 2023 High

    Established causal links between the CxxC-PRC1 axis and neurodevelopmental disease, and tied KDM2B/PRC1.1 to metabolic gene regulation via MYC/ATF4.

    Evidence CxxC-domain conditional KO/knock-in mice with ChIP-seq, RNA-seq, and behavioral phenotyping; multi-omics in TNBC cells; CxxC-variant DNA-binding functional assays in patient cohort

    PMID:35128353 PMID:37838801 PMID:37935302 PMID:40420380

    Open questions at the time
    • distinction between CxxC-variant syndrome and haploinsufficiency mechanism still being defined
    • tissue-specific selection of KDM2B target programs not resolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How KDM2B selects among its mutually exclusive activities — JmjC demethylation, PRC1.1 scaffolding, and SCF-type ubiquitin ligation — at specific loci and in specific cell types, and which reported histone substrates (H3K4me3, H3K79, H3K9) are bona fide in vivo, remain unresolved.
  • no unified model partitioning catalytic vs scaffold functions
  • conflicting substrate assignments across labs
  • regulation of PRC1.1-vs-SCF assembly switching unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 5 GO:0003677 DNA binding 4 GO:0140110 transcription regulator activity 4 GO:0016491 oxidoreductase activity 3 GO:0016874 ligase activity 2 GO:0042393 histone binding 1
Localization
GO:0005634 nucleus 3 GO:0000228 nuclear chromosome 2 GO:0005730 nucleolus 1
Pathway
R-HSA-1266738 Developmental Biology 4 R-HSA-4839726 Chromatin organization 4 R-HSA-74160 Gene expression (Transcription) 4 R-HSA-1643685 Disease 3 R-HSA-392499 Metabolism of proteins 1 R-HSA-73894 DNA Repair 1
Partners
BCOR/BCORL1BRG1EZH2PARP1PCGF1/NSPC1RING1B/RNF2SKP1TIMELESS
Complex memberships
FRRUC (FBXL10-RNF68-RNF2)PRC1.1 (noncanonical PRC1)SCF^KDM2B (CRL1) E3 ubiquitin ligase

Evidence

Reading pass · 46 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2012 KDM2B (FBXL10) specifically recognizes non-methylated CpG island DNA via its CxxC domain and recruits Polycomb Repressive Complex 1 (PRC1), contributing to histone H2A lysine 119 ubiquitylation (H2AK119ub1) and gene repression. CGIs are occupied by low levels of KDM2B-PRC1 complex genome-wide, suggesting a sampling mechanism for polycomb-mediated silencing. ChIP-seq, genome-wide binding analysis, Co-IP, functional domain analysis in mouse ESCs eLife High 23256043
2013 Fbxl10/KDM2B interacts with Ring1B and Nspc1 to form a noncanonical PRC1 complex required for H2AK119ub1 in mouse ESCs. Both its DNA-binding capability and integration into PRC1 are required for H2AK119 ubiquitylation; Fbxl10 depletion causes a major loss of H2AK119ub1 and decreased Ring1B binding to target genes. Co-IP, genome-wide ChIP-seq, genetic loss-of-function with domain mutants in mouse ESCs Molecular cell High 23395003
2013 Kdm2b maintains mESC undifferentiated state by binding CpG islands genome-wide via its CxxC-ZF domain, interacting with core PRC1 components, and recruiting PRC1 to CGIs of early lineage-specific genes to repress their expression. Oct4 and Sox2 directly regulate Kdm2b expression. Co-IP, ChIP-seq, domain deletion/mutant analysis, shRNA knockdown, gene expression profiling in mESCs Nature cell biology High 23502314
2008 Jhdm1b/KDM2B is a histone H3 lysine 36 (H3K36) demethylase. Knockdown in primary MEFs inhibits cell proliferation and induces cellular senescence in a pRb- and p53-dependent manner. KDM2B targets the p15(Ink4b) locus and regulates its expression in an enzymatic activity-dependent manner; loss of p15(Ink4b) rescues proliferation defects caused by KDM2B knockdown. In vitro demethylase assay, ChIP, shRNA knockdown, genetic rescue experiments in MEFs Nature structural & molecular biology High 18836456
2007 JHDM1B/KDM2B localizes to the nucleolus, preferentially binds the transcribed region of ribosomal DNA, and represses rRNA gene transcription. Repression depends on the JmjC domain, which demethylates trimethylated H3K4 specifically in the nucleolus. JHDM1B negatively affects cell size and proliferation in a JmjC domain-dependent manner. Subcellular fractionation/immunofluorescence (nucleolar localization), ChIP, RNAi, in vitro demethylase assay Nature High 17994099
2007 Fbxl10/KDM2B forms a novel complex with Ring1B/Rnf2 that also contains BcoR, CK2alpha, Skp1, and Nspc1/Pcgf1, distinct from canonical PRC1. Identified by proteomics/mass spectrometry purification of biotinylated Ring1B. In vivo biotinylation tagging, streptavidin pulldown, mass spectrometry identification Molecular & cellular proteomics : MCP Medium 17296600
2016 Crystal structure of the KDM2B/SKP1/BCORL1/PCGF1 tetrameric complex was solved. The BCORL1 PUFD domain positions residues preceding the RAWUL domain of PCGF1 to create an extended interface for interaction with KDM2B unique to PRC1.1. This also reveals how KDM2B may simultaneously function in PRC1.1 and SCF ubiquitin ligase complex. In vitro complex assembly, crystal structure determination Structure (London, England : 1993) High 27568929
2009 Ndy1/KDM2B represses the Ink4a/Arf locus through a JmjC domain-dependent process: it counteracts senescence-associated down-regulation of Ezh2 (PRC2), leading to global and locus-specific up-regulation of H3K27me3, which promotes Bmi1 (PRC1) binding at the Ink4a/Arf locus. KDM2B also demethylates locus-associated H3K36me2 and H3K4me3 and binds Ezh2. ChIP, Co-IP (KDM2B-Ezh2 interaction), shRNA knockdown, histone modification analysis in MEFs Proceedings of the National Academy of Sciences of the United States of America Medium 19202064
2011 KDM2B/JHDM1b functions as an H3K36 dimethyl-specific demethylase and is required for leukemic transformation. Ectopic Kdm2b transforms hematopoietic progenitors; its knockdown impairs Hoxa9/Meis1-induced leukemia. The mechanism requires active H3K36me2 demethylation to silence p15(Ink4b) in leukemic stem cells. Retroviral overexpression, shRNA knockdown, in vivo leukemia models, H3K36me2 demethylase activity assay, ChIP Blood High 21310926
2011 KDM2B is induced by FGF-2 via CREB phosphorylation downstream of DYRK1A. KDM2B and EZH2 co-bind the miR-101 promoter and repress it; KDM2B binding is independent of EZH2 but EZH2 binding depends on KDM2B. This NDY1/KDM2B-miR-101-EZH2 positive feedback axis mediates FGF-2 effects on cell proliferation, migration, and angiogenesis. ChIP, Co-IP, shRNA knockdown, luciferase reporter assays, signaling pathway analysis Molecular cell Medium 21777817
2011 KDM2B silences let-7b and miR-101 through locus-specific H3K36me2 demethylation, preventing these miRNAs from targeting EZH2 mRNA; this upregulates EZH2 and promotes immortalization of MEFs. The KDM2B-let-7-EZH2 pathway also promotes proliferation of Ink4a/Arf null fibroblasts. ChIP, shRNA knockdown, miRNA overexpression/inhibition, epistasis experiments in MEFs The Journal of biological chemistry Medium 21757686
2012 Kdm2b promotes iPSC generation by binding to and demethylating H3K36me2 at early responsive gene promoters, enhancing their activation early in reprogramming. This capacity depends on both demethylase and DNA-binding activities and is largely independent of its anti-senescence role. Retroviral overexpression, domain mutant analysis, ChIP, gene expression profiling during reprogramming Nature cell biology Medium 22522173
2015 Complete inactivation of Fbxl10 leads to dense de novo methylation specifically at promoters co-occupied by both FBXL10 and Polycomb repressive complexes, causing embryonic lethality at midgestation. FBXL10 thus protects Polycomb-bound promoters against ectopic de novo DNA methylation; deletion of PRC1/PRC2 components alone did not lead to ectopic methylation. Conditional/complete gene knockout in mice, whole-genome bisulfite sequencing, ChIP Nature genetics High 25848754
2007 Fbl10/KDM2B interacts with c-Jun, is present at the c-jun promoter (dependent on c-Jun recruitment), binds unmethylated CpG sequences via its CxxC zinc finger, and tethers transcriptional repressor complexes to repress c-Jun-mediated transcription. Fbl10 is downregulated by UV irradiation inversely with c-Jun induction. ChIP, Co-IP, CxxC domain DNA-binding assay, RNAi, cell-cycle and apoptosis assays Nature cell biology Medium 17704768
2013 KDM2B drives pancreatic cancer tumorigenicity via two transcriptional mechanisms: (1) repression of developmental genes by co-binding with Polycomb group proteins at transcriptional start sites; (2) activation of metabolic genes (protein synthesis, mitochondrial function) co-bound by MYC and KDM5A. Both loss- and gain-of-function experiments linked to genome-wide ChIP-seq confirmed these programs. ChIP-seq, genome-wide gene expression, gain/loss-of-function experiments, mouse PDAC model The Journal of clinical investigation High 23321669
2018 SS18-SSX1 oncoprotein physically interacts with PRC1.1 (containing KDM2B) and co-associates with SWI/SNF and KDM2B complexes on unmethylated CpG islands. Via KDM2B, SS18-SSX1 aberrantly activates polycomb-repressed developmental genes; KDM2B depletion restores repression and leads to irreversible mesenchymal differentiation. Co-IP, ChIP-seq, shRNA depletion, functional genomics in synovial sarcoma cells Cancer cell High 29502955
2016 KDM2B, via its F-box domain, assembles an SCF (CRL1/SCF^KDM2B) E3 ubiquitin ligase complex and targets c-Fos for polyubiquitylation and degradation. EGF-induced c-Fos S374 phosphorylation dissociates c-Fos from KDM2B, stabilizing c-Fos; tumor-derived KDM2B mutations impair c-Fos degradation. Co-IP, ubiquitylation assay, mutagenesis (S374), cell proliferation assays, tumor mutation analysis Oncogene High 26725323
2018 KDM2B is a di- and trimethyl H3K79 demethylase in addition to its H3K36 activity. KDM2B occupies promoters of HOXA7 and MEIS1 and induces their transcriptional repression via H3K79 demethylation. KDM2B knockdown increases genome-wide H3K79 methylation, and KDM2B-depleted cells show displacement of SIRT1 from chromatin with concomitant increases in H3K79me and H4K16ac. In vitro demethylase assay, ChIP, genome-wide H3K79 methylation analysis, SIRT1 displacement assay FASEB journal Medium 29763382
2018 The FBXL10-RNF68-RNF2 ubiquitin ligase complex (FRRUC) is rapidly and transiently recruited to DNA damage sites in a PARP1- and TIMELESS-dependent manner. At damage sites, FRRUC promotes H2AK119 mono-ubiquitylation, local H2A decrease, and H2A.Z incorporation, facilitating transcriptional repression, DSB signaling, and homologous recombination repair. FRRUC activity is required for proper recruitment of BMI1-RNF2 and MEL18-RNF2 complexes upon genotoxic stress. Live-cell imaging (FRAP/recruitment kinetics), ChIP, Co-IP, genetic depletion with HR assay, H2A.Z incorporation assay eLife High 29985131
2014 NDY1/KDM2B functions as a master regulator of PRC1 and PRC2 miRNA targets by repressing miRNAs that target polycomb complex members. Its knockdown de-represses these miRNAs, downregulating polycomb proteins. KDM2B is required for self-renewal of breast cancer stem cells (mammosphere formation, ALDH/CD44 markers), and its knockdown induces differentiation. shRNA knockdown, mammosphere assay, FACS for stem markers, miRNA profiling, rescue experiments Cancer research Medium 24853546
2016 FBXL10/KDM2B inhibits adipogenesis via its F-box and leucine-rich repeat domains by recruiting a noncanonical PRC1 (containing RING1B, SKP1, PCGF1, and BCOR). Knockdown of RING1B or SKP1 prevents FBXL10-mediated repression of adipogenesis. ChIP-seq shows FBXL10 recruits RING1B to loci surrounding Cdk1, Uhrf1, and Pparg genes. The JmjC demethylase domain is not required for this function. ChIP-seq, Co-IP, domain deletion analysis (F-box/LRR vs JmjC), shRNA knockdown, adipogenesis assay The Journal of biological chemistry Medium 25533466
2019 KDM2B promotes IL-6 production by binding the Il6 promoter and interacting with Brg1 (SWI/SNF ATPase) to facilitate chromatin accessibility, and directly recruits RNA Polymerase II to initiate Il6 transcription. This function is independent of its demethylase activity. KDM2B-deficient mice show reduced IL-6 and resistance to endotoxin shock. ChIP, Co-IP (KDM2B-Brg1), ATAC-seq/chromatin accessibility, conditional KO mice, ELISA Cellular & molecular immunology Medium 31197256
2012 Fbxl10 acts as an H3K4me3 demethylase (rather than primarily H3K36me2) based on in vitro purification and biochemical assays of its JmjC domain. Its PHD domain exhibits dual function: binding H3K4me3 and H3K36me2 AND exhibiting E3 ubiquitin ligase activity. Fbxl10 is recruited to Ccl7, Xist, Crabp2, and RipK3 promoters with reduced H3K4me3 but unchanged H3K36me2. In vitro demethylase assay with purified JmjC domain, PHD domain E3 ligase assay, ChIP, ChIP-seq The Journal of biological chemistry Low 22825849
2021 KDM2B demethylates the non-histone substrate serum response factor (SRF) at K165, negatively regulating muscle differentiation. The methyltransferase SET7 counteracts KDM2B by methylating SRF K165, which is required for transcriptional activation of SRF-dependent muscle genes. Both KDM2B and SET7 regulate the balance of SRF K165 methylation. Co-IP, in vitro demethylase assay on SRF substrate, ChIP, muscle differentiation assays, SET7 inhibitor experiments Experimental & molecular medicine Medium 33564100
2019 Tip60 acetylates KDM2B at lysine 758 in osteosarcoma cells. Acetylation of KDM2B decreases its capacity to bind nucleosomes and diminishes its demethylase activity toward nucleosomal (but not bulk histone) substrates, reducing its binding to p21 and PUMA promoters and enhancing its oncogenic effects. Co-IP, in vitro demethylase assay (nucleosomal substrate), acetylation mutagenesis (K758), ChIP, tumor growth assays Journal of cellular and molecular medicine Medium 31218831
2020 KDM2B directly suppresses let-7b expression via H3K36me2 demethylation at the let-7b locus in ovarian cancer cells, thereby allowing EZH2 upregulation (let-7b targets EZH2). This KDM2B-let-7b-EZH2 axis promotes cancer cell proliferation and migration. ChIP (H3K36me2 at let-7b locus), let-7b overexpression rescue, EZH2 knockdown epistasis, xenograft model Cancer science Medium 33091189
2017 Kdm2b promotes Oct4-induced somatic reprogramming through recruitment of variant PRC1.1 complex to CpG islands. BMP-SMAD signaling attenuates PRC1.1 occupation and H2AK119 ubiquitination at developmental genes, enabling mesendodermal factor expression that suppresses reprogramming. ChIP-seq, Co-IP, domain mutant rescue, BMP signaling inhibition/activation experiments Cell reports Medium 29166607
2016 KDM2B cooperates with polycomb and trithorax complexes to regulate hematopoietic lineage commitment, differentiation, cytokine signaling, and cell cycle. KDM2B maintains lymphoid leukemias but restrains RAS-driven myeloid transformation, demonstrating context-dependent opposing roles. Kdm2b conditional KO mice, RNA-seq of HSPCs, ChIP-seq in human leukemias The Journal of clinical investigation Medium 26808549
2018 EBNA3C (EBV) physically interacts with KDM2B, and this interaction is important for removal of H3K4me3 at EBNA3C target genes (COBLL1, ADAM28-ADAMDEC1 locus), contributing to transcriptional repression. Full COBLL1 repression requires both H3K4me3 removal (via KDM2B interaction) and H3K27me3 deposition (via Polycomb recruitment). Co-IP (EBNA3C-KDM2B), ChIP (H3K4me3, H3K27me3), recombinant EBV with RBPJ interaction motif mutations Journal of virology Medium 30135119
2020 KDM2B-mediated H3K79 demethylation regulates cell cycle progression by controlling timely PCNA dissociation from chromatin during S phase. PCNA binds chromatin in an H3K79me-dependent manner; KDM2B depletion causes aberrant PCNA retention on chromatin and slowed DNA replication. KDM2B depletion in 293T cells, H3K79R mutant histone, Co-IP, peptide pulldown, ITC, ChIP, iPOND, DNA fiber assay, flow cytometry Cell proliferation Medium 33029857
2019 ELKS1 stabilizes Kdm2b protein in mast cells; Kdm2b is an essential regulator of STX4 (Syntaxin 4) and Stxbp2 transcription required for mast cell degranulation. Loss of ELKS1 reduces Kdm2b stability, decreasing STX4/Stxbp2 transcription and impairing degranulation both in vivo and in vitro. Mast cell-specific ELKS1 knockout mice, Co-IP (ELKS1-Kdm2b), ChIP (Kdm2b at STX4/Stxbp2 promoters), degranulation assays Science advances Medium 32937583
2015 Fbxl10 directly binds regulatory regions of Nsg2 and oxidative phosphorylation genes, upregulating their expression. Fbxl10 overexpression in HSCs leads to G0/G1-to-S transition acceleration, progenitor cell expansion, and development of myeloid or B-lymphoid leukemia with complete penetrance in transgenic mice. ChIP-seq, transgenic mouse model (HSC-specific overexpression), gene expression analysis, metabolic profiling Blood Medium 25872778
2011 Fbxl10 deficiency causes increased apoptosis in neuroepithelium and mesenchyme during embryonic development, associated with increased p19ARF expression, leading to neural tube defects and exencephaly. Fbxl10 thus regulates cell proliferation and death in neural progenitors via p19ARF suppression. Fbxl10 knockout mouse generation, in situ hybridization, apoptosis analysis (TUNEL), p19ARF expression analysis Molecular and cellular neurosciences Medium 21220025
2016 Alternative short isoforms of KDM2B (KDM2B-SF), lacking the N-terminal demethylase domain, bind CpG island promoters of Wnt target genes (Axin2, Cyclin D1) and repress their expression. KDM2B-SF interacts with TCF7L1, a Wnt transcriptional mediator, to repress Wnt-responsive transcription. The DNA-binding domain is required for this repression; the demethylase domain is dispensable. Luciferase reporter assay (Wnt-responsive), ChIP at Axin2/CyclinD1 promoters, Co-IP (KDM2B-SF with TCF7L1), isoform overexpression PloS one Medium 33104714
2023 KDM2B, via its chromatin-association (CxxC) domain, transcriptionally silences Wnt signaling genes in hippocampal neural progenitors. Loss of the CxxC domain reduces polycomb repressive complex enrichment at Wnt gene loci, de-repressing Wnt signaling, impairing neural progenitor migration/differentiation, and causing hippocampal hypoplasia and spatial memory deficits. Conditional CxxC-domain deletion mouse (Kdm2b^ΔCxxC), ChIP-seq (PRC marks), RNA-seq, behavioral testing Nature communications High 37838801
2022 Loss of the CxxC-ZF domain of KDM2B impairs PRC1 recruitment to chromatin in neural stem cells, causing de-repression of apoptosis/cell-cycle-arrest/senescence genes, loss of NSC populations, and ASD/ID-like behavioral deficits in mice. Establishes causality between KDM2B-PRC1 chromatin regulation and ASD/ID-like phenotypes. Kdm2b CxxC-domain knock-in mouse, ChIP (PRC1 occupancy), RNA-seq, behavioral phenotyping iScience High 35128353
2025 CxxC domain variants of KDM2B significantly reduce its DNA-binding ability without affecting protein expression, causing a distinct neurodevelopmental syndrome (developmental delay, congenital heart defects, intellectual disability) that differs clinically from haploinsufficiency. Functional assays confirm reduced DNA binding as the mechanism for CxxC-variant pathogenicity. DNA-binding assay (functional assay with CxxC mutants), protein expression assays, cohort clinical analysis Human molecular genetics Medium 40420380
2021 KDM2B promotes IL-6-mediated inflammatory responses in macrophages by interacting with Brg1 (SWI/SNF). KDM2B knockdown in macrophages reduces IL-6 but not TNF-α, IL-1, or IFN-β, and KDM2B-deficient mice resist endotoxin shock with decreased IL-6. KDM2B conditional KO mice, ChIP (KDM2B at Il6 promoter), Co-IP (KDM2B-Brg1), ELISA Inflammation Low 31041569
2021 FBXL10 stabilizes ERRα protein by reducing its poly-ubiquitylation and promoting its mono-ubiquitylation, increasing ERRα transcriptional activity and ERRα enrichment at target gene promoters. FBXL10 facilitates ERRα/PGC1β-mediated proliferation and tumorigenesis in breast cancer. Co-IP (FBXL10-ERRα), ubiquitylation assay, reporter gene assay, ChIP (ERRα at target promoters), in vitro/in vivo proliferation assays Cancer letters Medium 33450359
2021 FBXL10 promotes EMT in breast cancer by interacting specifically with SNAI1 (not Slug or ZEB1), enhancing SNAI1 transcriptional repression of CDH1 by facilitating the interaction between SNAI1 and HDAC1, thereby promoting SNAI1 deacetylation. Deacetylated SNAI1 more potently suppresses E-cadherin transcription. Co-IP (FBXL10-SNAI1, SNAI1-HDAC1), reporter assay (CDH1 promoter), in vitro/in vivo migration/invasion assays, mouse lung metastasis model Cell death discovery Medium 34718323
2023 KDM2B, functioning in the context of ncPRC1.1, regulates amino acid metabolism including SGOC, glutamate, and GSH pathways by enhancing chromatin accessibility and expression of MYC and ATF4. KDM2B co-occupies promoters of transcriptionally active metabolic genes together with MYC and ATF4, and regulates the expression and transcriptional activity of MYC. ChIP-seq, ATAC-seq, RNA-seq, TMT proteomics, global metabolomics, shRNA knockdown in TNBC cells Metabolism: clinical and experimental Medium 37935302
2023 DHX9 (DNA/RNA helicase) collaborates with KDM2B to regulate YAP1 expression in Ewing sarcoma. DHX9 enhances H3K9 chromatin demethylation by KDM2B and favors RNA Polymerase II recruitment to the YAP1 promoter. EWS-FLI1 binding to the YAP1 promoter antagonizes this activation. Co-IP (DHX9-KDM2B), ChIP (H3K9me, RNA Pol II), RNA-seq, shRNA depletion Oncogene Low 38017132
2020 KDM2B overexpression activates FAK signaling and PI3K (p85 subunit upregulation) in prostate and colon cancer cells, promoting cell migration. KDM2B depletion reduces FAK activity and p85-PI3K without altering FAK gene expression/protein levels. KDM2B-driven migration is abolished by PI3K inhibitor LY294002. Western blot (FAK/PI3K activity), shRNA knockdown, wound-healing migration assay, LY294002 inhibition Cancer biology & therapy Low 32175798
2019 KDM2B is required for KDM2B-mediated transcriptional repression of NOTCH1 target genes in T-cell leukemia via PRC1.1. Kdm2b-deficient mice (lacking the CxxC domain) develop NOTCH1-dependent T-ALL, similar to Bcor-deficient mice, indicating PRC1.1 restricts excessive NOTCH1-mediated gene activation as a tumor suppressor. CxxC-domain specific KO mice, ChIP-seq (KDM2B, BCOR, EZH2, H2AK119ub1, H3K4me3, H3K27me3), RNA-seq, T-ALL mouse model Blood advances High 31471323
2020 KDM2B regulates KDM2B-mediated H2AK119 monoubiquitination as a component of PRC1 to repress CDH1, miR200a, and CGN during TGF-β-induced EMT. KDM2B recruits EZH2 and induces H3K27 methylation at these loci. The DNA-recognition property (CxxC domain) but not demethylase activity is required for this function. ChIP (H2AK119ub1, EZH2 recruitment), KDM2B domain mutants, shRNA knockdown, morphological EMT assays The Journal of biological chemistry Medium 33779563
2021 KDM2B directly binds the promoter region of MOB1 and suppresses its promoter activity, transcriptionally inhibiting MOB1 expression to regulate the Hippo pathway and promote PDAC proliferation/migration/invasion. ChIP (KDM2B at MOB1 promoter), luciferase reporter assay (MOB1 promoter), shRNA knockdown, rescue experiments Journal of experimental & clinical cancer research : CR Medium 31941533

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 KDM2B links the Polycomb Repressive Complex 1 (PRC1) to recognition of CpG islands. eLife 370 23256043
2013 Fbxl10/Kdm2b recruits polycomb repressive complex 1 to CpG islands and regulates H2A ubiquitylation. Molecular cell 299 23395003
2013 Kdm2b maintains murine embryonic stem cell status by recruiting PRC1 complex to CpG islands of developmental genes. Nature cell biology 254 23502314
2008 The H3K36 demethylase Jhdm1b/Kdm2b regulates cell proliferation and senescence through p15(Ink4b). Nature structural & molecular biology 247 18836456
2007 JHDM1B/FBXL10 is a nucleolar protein that represses transcription of ribosomal RNA genes. Nature 223 17994099
2007 Proteomics analysis of Ring1B/Rnf2 interactors identifies a novel complex with the Fbxl10/Jhdm1B histone demethylase and the Bcl6 interacting corepressor. Molecular & cellular proteomics : MCP 184 17296600
2011 FGF-2 regulates cell proliferation, migration, and angiogenesis through an NDY1/KDM2B-miR-101-EZH2 pathway. Molecular cell 183 21777817
2011 KDM2b/JHDM1b, an H3K36me2-specific demethylase, is required for initiation and maintenance of acute myeloid leukemia. Blood 162 21310926
2013 KDM2B promotes pancreatic cancer via Polycomb-dependent and -independent transcriptional programs. The Journal of clinical investigation 146 23321669
2012 Kdm2b promotes induced pluripotent stem cell generation by facilitating gene activation early in reprogramming. Nature cell biology 140 22522173
2015 FBXL10 protects Polycomb-bound genes from hypermethylation. Nature genetics 119 25848754
2018 The SS18-SSX Oncoprotein Hijacks KDM2B-PRC1.1 to Drive Synovial Sarcoma. Cancer cell 109 29502955
2009 Ndy1/KDM2B immortalizes mouse embryonic fibroblasts by repressing the Ink4a/Arf locus. Proceedings of the National Academy of Sciences of the United States of America 108 19202064
2011 Lysine-specific demethylase 2B (KDM2B)-let-7-enhancer of zester homolog 2 (EZH2) pathway regulates cell cycle progression and senescence in primary cells. The Journal of biological chemistry 105 21757686
2011 Fbxl10/Kdm2b deficiency accelerates neural progenitor cell death and leads to exencephaly. Molecular and cellular neurosciences 103 21220025
2018 KDM2B is a histone H3K79 demethylase and induces transcriptional repression via sirtuin-1-mediated chromatin silencing. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 78 29763382
2014 NDY1/KDM2B functions as a master regulator of polycomb complexes and controls self-renewal of breast cancer stem cells. Cancer research 74 24853546
2016 Histone demethylase KDM2B regulates lineage commitment in normal and malignant hematopoiesis. The Journal of clinical investigation 68 26808549
2012 The H3K4me3 histone demethylase Fbxl10 is a regulator of chemokine expression, cellular morphology, and the metabolome of fibroblasts. The Journal of biological chemistry 67 22825849
2018 HPV16 E6 and E7 upregulate the histone lysine demethylase KDM2B through the c-MYC/miR-146a-5p axys. Oncogene 60 29335520
2018 The critical role of histone lysine demethylase KDM2B in cancer. American journal of translational research 60 30210666
2018 Targeting glioma stem-like cell survival and chemoresistance through inhibition of lysine-specific histone demethylase KDM2B. Molecular oncology 56 29360266
2016 An atypical 12q24.31 microdeletion implicates six genes including a histone demethylase KDM2B and a histone methyltransferase SETD1B in syndromic intellectual disability. Human genetics 55 27106595
2007 The F-box protein Fbl10 is a novel transcriptional repressor of c-Jun. Nature cell biology 51 17704768
2016 KDM2B Recruitment of the Polycomb Group Complex, PRC1.1, Requires Cooperation between PCGF1 and BCORL1. Structure (London, England : 1993) 50 27568929
2015 Fbxl10 overexpression in murine hematopoietic stem cells induces leukemia involving metabolic activation and upregulation of Nsg2. Blood 49 25872778
2018 PARP1-dependent recruitment of the FBXL10-RNF68-RNF2 ubiquitin ligase to sites of DNA damage controls H2A.Z loading. eLife 46 29985131
2019 KDM2B promotes IL-6 production and inflammatory responses through Brg1-mediated chromatin remodeling. Cellular & molecular immunology 45 31197256
2019 Induction of Pluripotent Stem Cells from Mouse Embryonic Fibroblasts by Jdp2-Jhdm1b-Mkk6-Glis1-Nanog-Essrb-Sall4. Cell reports 44 31216469
2016 KDM2B/FBXL10 targets c-Fos for ubiquitylation and degradation in response to mitogenic stimulation. Oncogene 41 26725323
2017 Decreased miR-146a expression in acute ischemic stroke directly targets the Fbxl10 mRNA and is involved in modulating apoptosis. Neurochemistry international 40 28202285
2017 Histone demethylase KDM2B upregulates histone methyltransferase EZH2 expression and contributes to the progression of ovarian cancer in vitro and in vivo. OncoTargets and therapy 40 28706445
2016 MiR-448 promotes glycolytic metabolism of gastric cancer by downregulating KDM2B. Oncotarget 39 26989077
2011 Forced expression of the histone demethylase Fbxl10 maintains self-renewing hematopoietic stem cells. Experimental hematology 36 21540074
2019 Long non-coding RNA LncKdm2b regulates cortical neuronal differentiation by cis-activating Kdm2b. Protein & cell 35 31317506
2017 KDM2B, an H3K36-specific demethylase, regulates apoptotic response of GBM cells to TRAIL. Cell death & disease 34 28661478
2014 The FBXL10/KDM2B scaffolding protein associates with novel polycomb repressive complex-1 to regulate adipogenesis. The Journal of biological chemistry 34 25533466
2017 Kdm2b Regulates Somatic Reprogramming through Variant PRC1 Complex-Dependent Function. Cell reports 33 29166607
2013 Knockdown of fbxl10/kdm2bb rescues chd7 morphant phenotype in a zebrafish model of CHARGE syndrome. Developmental biology 33 23920116
2018 miR-146b promotes cell proliferation and increases chemosensitivity, but attenuates cell migration and invasion via FBXL10 in ovarian cancer. Cell death & disease 32 30409964
2021 The Role of KDM2B and EZH2 in Regulating the Stemness in Colorectal Cancer Through the PI3K/AKT Pathway. Frontiers in oncology 31 33791221
2017 Inhibition of cell proliferation and induction of autophagy by KDM2B/FBXL10 knockdown in gastric cancer cells. Cellular signalling 31 28506929
2022 Delineation of a KDM2B-related neurodevelopmental disorder and its associated DNA methylation signature. Genetics in medicine : official journal of the American College of Medical Genetics 29 36322151
2018 The epigenetic factor KDM2B regulates cell adhesion, small rho GTPases, actin cytoskeleton and migration in prostate cancer cells. Biochimica et biophysica acta. Molecular cell research 26 29408056
2014 The KDM2B- let-7b -EZH2 axis in myelodysplastic syndromes as a target for combined epigenetic therapy. PloS one 25 25225797
2020 Inhibition of microRNA let-7b expression by KDM2B promotes cancer progression by targeting EZH2 in ovarian cancer. Cancer science 24 33091189
2018 Histone demethylase KDM2B promotes triple negative breast cancer proliferation by suppressing p15INK4B, p16INK4A, and p57KIP2 transcription. Acta biochimica et biophysica Sinica 24 30060056
2019 KDM2B in polycomb repressive complex 1.1 functions as a tumor suppressor in the initiation of T-cell leukemogenesis. Blood advances 22 31471323
2021 FBXL10 promotes ERRα protein stability and proliferation of breast cancer cells by enhancing the mono-ubiquitylation of ERRα. Cancer letters 21 33450359
2020 Lysine demethylase 2 (KDM2B) regulates hippo pathway via MOB1 to promote pancreatic ductal adenocarcinoma (PDAC) progression. Journal of experimental & clinical cancer research : CR 21 31941533
2016 The Histone Demethylase FBXL10 Regulates the Proliferation of Spermatogonia and Ensures Long-Term Sustainable Spermatogenesis in Mice. Biology of reproduction 21 26984996
2021 Genome-wide screens uncover KDM2B as a modifier of protein binding to heparan sulfate. Nature chemical biology 20 33846619
2017 Epigenetic up-regulation of ribosome biogenesis and more aggressive phenotype triggered by the lack of the histone demethylase JHDM1B in mammary epithelial cells. Oncotarget 20 28415746
2014 RETRACTED: The downregulation of GFI1 by the EZH2-NDY1/KDM2B-JARID2 axis and by human cytomegalovirus (HCMV) associated factors allows the activation of the HCMV major IE promoter and the transition to productive infection. PLoS pathogens 20 24830456
2020 KDM2B is involved in the epigenetic regulation of TGF-β-induced epithelial-mesenchymal transition in lung and pancreatic cancer cell lines. The Journal of biological chemistry 18 33779563
2018 The Epigenetic Factor KDM2B Regulates EMT and Small GTPases in Colon Tumor Cells. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 17 29772566
2016 Abnormal X chromosome inactivation and sex-specific gene dysregulation after ablation of FBXL10. Epigenetics & chromatin 17 27252784
2014 JHDM1B expression regulates ribosome biogenesis and cancer cell growth in a p53 dependent manner. International journal of cancer 17 25273595
2019 FBXL10 regulates cardiac dysfunction in diabetic cardiomyopathy via the PKC β2 pathway. Journal of cellular and molecular medicine 16 30701683
2021 SRF is a nonhistone methylation target of KDM2B and SET7 in the regulation of skeletal muscle differentiation. Experimental & molecular medicine 15 33564100
2021 KDM2B promotes cell viability by enhancing DNA damage response in canine hemangiosarcoma. Journal of genetics and genomics = Yi chuan xue bao 15 34023294
2019 Protective effect of FBXL10 in myocardial ischemia reperfusion injury via inhibiting endoplasmic reticulum stress. Respiratory medicine 15 32056726
2018 FBXL10 contributes to the development of diffuse large B-cell lymphoma by epigenetically enhancing ERK1/2 signaling pathway. Cell death & disease 15 29352142
2012 KDM2B is implicated in bovine lethal multi-organic developmental dysplasia. PloS one 15 23029151
2019 Tip60-dependent acetylation of KDM2B promotes osteosarcoma carcinogenesis. Journal of cellular and molecular medicine 14 31218831
2023 KDM2B regulates hippocampal morphogenesis by transcriptionally silencing Wnt signaling in neural progenitors. Nature communications 13 37838801
2021 Epigenetic changes related to glucose metabolism in type 1 diabetes after BCG vaccinations: A vital role for KDM2B. Vaccine 13 33933315
2021 FBXL10 promotes EMT and metastasis of breast cancer cells via regulating the acetylation and transcriptional activity of SNAI1. Cell death discovery 12 34718323
2020 ELKS1 controls mast cell degranulation by regulating the transcription of Stxbp2 and Syntaxin 4 via Kdm2b stabilization. Science advances 12 32937583
2015 A systematic study of the cellular metabolic regulation of Jhdm1b in tumor cells. Molecular bioSystems 12 25877602
2023 Transcriptional regulation of amino acid metabolism by KDM2B, in the context of ncPRC1.1 and in concert with MYC and ATF4. Metabolism: clinical and experimental 11 37935302
2020 The histone demethylase KDM2B activates FAK and PI3K that control tumor cell motility. Cancer biology & therapy 11 32175798
2020 Histone H3K79 demethylation by KDM2B facilitates proper DNA replication through PCNA dissociation from chromatin. Cell proliferation 11 33029857
2020 Alternative isoforms of KDM2A and KDM2B lysine demethylases negatively regulate canonical Wnt signaling. PloS one 11 33104714
2019 Regulation of KDM2B and Brg1 on Inflammatory Response of Nasal Mucosa in CRSwNP. Inflammation 11 31041569
2015 Histone demethylase KDM2B inhibits the chondrogenic differentiation potentials of stem cells from apical papilla. International journal of clinical and experimental medicine 11 25932147
2023 KDM2B regulates inflammation and oxidative stress of sepsis via targeting NF-κB and AP-1 pathways. Immunity, inflammation and disease 10 37773725
2022 KDM2B mediates the Wnt/β-catenin pathway through transcriptional activation of PKMYT1 via microRNA-let-7b-5p/EZH2 to affect the development of non-small cell lung cancer. Experimental cell research 10 35580699
2021 Positional cloning and comprehensive mutation analysis identified a novel KDM2B mutation in a Japanese family with minor malformations, intellectual disability, and schizophrenia. Journal of human genetics 10 33402700
2021 Mutation and expression alterations of histone methylation-related NSD2, KDM2B and SETMAR genes in colon cancers. Pathology, research and practice 10 33621919
2019 KDM2B regulates choline kinase expression and neuronal differentiation of neuroblastoma cells. PloS one 10 30629659
2019 Induction of co-inhibitory molecule CTLA-4 by human papillomavirus E7 protein through downregulation of histone methyltransferase JHDM1B expression. Virology 10 31590057
2016 Enhanced direct conversion of fibroblasts into hepatocyte-like cells by Kdm2b. Biochemical and biophysical research communications 10 27103435
2024 KDM2B regulates stroke injury by modulating OGT-mediated 0-GlcNAcylation of SLC7A11. Communications biology 9 39558086
2023 KDM2B-Rearranged Soft Tissue Sarcomas Expand the Concept of BCOR-Associated Sarcoma. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 9 37634866
2022 Impaired KDM2B-mediated PRC1 recruitment to chromatin causes defective neural stem cell self-renewal and ASD/ID-like behaviors. iScience 9 35128353
2021 Knockdown of lysine (K)-specific demethylase 2B KDM2B inhibits glycolysis and induces autophagy in lung squamous cell carcinoma cells by regulating the phosphatidylinositol 3-kinase/AKT/mammalian target of rapamycin pathway. Bioengineered 9 34783291
2021 KDM2B overexpression prevents myocardial ischemia-reperfusion injury in rats through regulating inflammatory response via the TLR4/NF-κB p65 axis. Experimental and therapeutic medicine 9 35069835
2018 Epstein-Barr Virus Nuclear Antigen 3C Inhibits Expression of COBLL1 and the ADAM28-ADAMDEC1 Locus via Interaction with the Histone Lysine Demethylase KDM2B. Journal of virology 9 30135119
2015 FBXL10 contributes to the progression of nasopharyngeal carcinoma via involving in PI3K/mTOR pathway. Neoplasma 9 26458315
2020 KDM2B-associated paunch calf syndrome in Marchigiana cattle. Journal of veterinary internal medicine 7 32515858
2025 SAMD4A inhibits abdominal aortic aneurysm development and VSMC phenotypic transformation through targeting KDM2B. Journal of advanced research 6 40081568
2023 The DNA/RNA helicase DHX9 orchestrates the KDM2B-mediated transcriptional regulation of YAP1 in Ewing sarcoma. Oncogene 6 38017132
2021 Oncogenic role of ALX3 in cervical cancer cells through KDM2B-mediated histone demethylation of CDC25A. BMC cancer 6 34266408
2024 CircMAPK1 induces cell pyroptosis in sepsis-induced lung injury by mediating KDM2B mRNA decay to epigenetically regulate WNK1. Molecular medicine (Cambridge, Mass.) 5 39300342
2024 KDM2B and its peptides promote the stem cells from apical papilla mediated nerve injury repair in rats by intervening EZH2 function. Cell proliferation 5 39358887
2021 KDM2B Overexpression Facilitates Lytic De Novo KSHV Infection by Inducing AP-1 Activity Through Interaction with the SCF E3 Ubiquitin Ligase Complex. Journal of virology 5 33692209
2016 Overexpression of histone demethylase Fbxl10 leads to enhanced migration in mouse embryonic fibroblasts. Experimental cell research 5 27646113
2022 MicroRNA-211-5p in extracellular vesicles derived from BMSCs facilitates the repair of rat frozen shoulder via regulating KDM2B/LACC1 axis. Tissue & cell 4 36610229
2025 KDM2B variants in the CxxC domain impair its DNA-binding ability and cause a distinct neurodevelopmental syndrome. Human molecular genetics 3 40420380

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