Affinage

KDM2B

Lysine-specific demethylase 2B · UniProt Q8NHM5

Length
1336 aa
Mass
152.6 kDa
Annotated
2026-04-28
100 papers in source corpus 45 papers cited in narrative 45 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

KDM2B is a multifunctional chromatin regulator that operates at the intersection of Polycomb-mediated gene silencing, histone demethylation, and ubiquitin ligase signaling to control cell fate decisions including pluripotency, differentiation, senescence, and DNA damage repair. Through its CxxC zinc-finger domain, KDM2B recognizes unmethylated CpG islands and recruits a noncanonical PRC1.1 complex (RING1B, PCGF1, BCOR/BCORL1, SKP1) that catalyzes H2AK119 monoubiquitylation to silence developmental and lineage-specific genes, a function essential for embryonic stem cell self-renewal, neural progenitor maintenance, hematopoietic differentiation, and protection of CpG island promoters from aberrant DNA methylation (PMID:23256043, PMID:23395003, PMID:23502314, PMID:25848754, PMID:35128353). Its JmjC domain demethylates H3K36me1/me2, H3K4me3, and H3K79me2/me3 at specific loci—including Ink4a/Arf, p15Ink4b, ribosomal RNA genes, and HOXA7—to regulate proliferation, senescence bypass, and transcriptional repression, while also acting as a non-histone demethylase targeting SRF K165 to modulate muscle differentiation (PMID:18836456, PMID:17994099, PMID:29763382, PMID:33564100). KDM2B additionally functions as an F-box subunit of an SCF E3 ubiquitin ligase that targets c-Fos for proteasomal degradation, is recruited to DNA double-strand breaks via PARP1/TIMELESS to promote H2AK119ub1-dependent homologous recombination repair, and its CxxC domain variants cause a neurodevelopmental syndrome (PMID:26725323, PMID:29985131, PMID:40420380).

Mechanistic history

Synthesis pass · year-by-year structured walk · 22 steps
  1. 2007 High

    Identification of KDM2B's core biochemical activities and interaction partners established it as both a histone demethylase and a PRC1-associated chromatin regulator, resolving what molecular functions this JmjC-domain protein performs.

    Evidence Proteomic identification of Ring1B/PCGF1/BCOR/SKP1 complex via biotin tagging and mass spectrometry; nucleolar localization and JmjC-dependent H3K4me3 demethylation at rDNA; CxxC-dependent binding to unmethylated CpG at the c-jun promoter with transcriptional repression

    PMID:17296600 PMID:17704768 PMID:17994099

    Open questions at the time
    • Catalytic specificity toward different histone marks not yet systematically compared
    • Whether demethylase and PRC1 functions act at the same or distinct loci was unclear
    • No structural basis for complex assembly
  2. 2008 High

    Establishing KDM2B as an H3K36me2 demethylase at the p15Ink4b locus linked its enzymatic activity to a defined cell proliferation/senescence regulatory pathway.

    Evidence In vitro histone demethylase assay, ChIP at p15Ink4b, shRNA knockdown with epistasis rescue

    PMID:18836456

    Open questions at the time
    • Whether H3K36me2 demethylation is sufficient or requires concurrent PRC1 activity at this locus
    • Substrate specificity in vivo beyond Ink4b not addressed
  3. 2009 High

    Demonstrating that KDM2B represses the Ink4a/Arf locus through a multi-layered mechanism—direct H3K36me2/H3K4me3 demethylation, indirect EZH2 stabilization, and Bmi1 recruitment—revealed how a single factor coordinates PRC1, PRC2, and demethylase activities to bypass senescence.

    Evidence ChIP for multiple histone marks, Co-IP for Ndy1-Ezh2, MEF immortalization with gain/loss-of-function

    PMID:19202064

    Open questions at the time
    • Relative contribution of each mechanism to senescence bypass not quantified
    • Whether EZH2 stabilization is direct or via miRNA-mediated mechanism not resolved
  4. 2011 High

    Clarifying the miRNA-mediated axis through which KDM2B maintains EZH2 levels (by silencing let-7b and miR-101 via H3K36me2 demethylation) and demonstrating KDM2B-EZH2 co-occupancy at miR-101 connected KDM2B's demethylase function to a broader Polycomb maintenance circuit.

    Evidence ChIP at miRNA loci, epistasis with let-7b overexpression, Co-IP and ChIP for KDM2B-EZH2 co-binding at miR-101 promoter, functional proliferation/migration assays

    PMID:21757686 PMID:21777817

    Open questions at the time
    • Whether EZH2 regulation is the primary or accessory function of KDM2B in proliferating cells
    • Generality of this miRNA axis beyond the cell types tested
  5. 2011 Medium

    In vivo knockout revealed that KDM2B is required for neural tube closure through regulation of p19ARF, establishing its physiological necessity in development beyond cultured cells.

    Evidence Fbxl10 knockout mouse, TUNEL and mitotic assays in neural progenitors, p19ARF qRT-PCR

    PMID:21220025

    Open questions at the time
    • Whether the neural tube phenotype reflects demethylase or PRC1 function not resolved
    • Contribution of other Ink4a/Arf locus products not fully dissected
  6. 2012 High

    Genome-wide demonstration that KDM2B's CxxC domain targets it to unmethylated CpG islands to recruit PRC1 and deposit H2AK119ub1 genome-wide resolved the long-standing question of how PRC1 finds its targets independently of PRC2.

    Evidence Genome-wide ChIP-seq for KDM2B and PRC1 components, CxxC domain binding assays, Co-IP

    PMID:23256043

    Open questions at the time
    • How CpG island targeting is modulated at different loci not addressed
    • Contribution of other CxxC-containing proteins to the same pathway
  7. 2012 High

    KDM2B's role in somatic cell reprogramming was shown to depend on H3K36me2 demethylation at early-responsive gene promoters rather than its anti-senescence activity, functionally separating its demethylase and Ink4a/Arf regulatory roles.

    Evidence Retroviral overexpression in reprogramming, demethylase-dead and DNA-binding mutant rescue, ChIP for H3K36me2 during reprogramming time course

    PMID:22522173

    Open questions at the time
    • Whether PRC1 recruitment also contributes to reprogramming efficiency
    • Generality beyond mouse reprogramming system
  8. 2013 High

    Defining the PRC1.1 complex composition and demonstrating its requirement for H2AK119ub1 in ESCs, combined with the finding that Oct4/Sox2 regulate Kdm2b transcription, placed KDM2B at the center of a core pluripotency-Polycomb regulatory circuit.

    Evidence Reciprocal Co-IP, genome-wide ChIP-seq in mESCs, knockdown/rescue with domain mutants

    PMID:23395003 PMID:23502314

    Open questions at the time
    • Redundancy with other ncPRC1 complexes in ESCs not fully resolved
    • How Kdm2b expression is regulated beyond Oct4/Sox2
  9. 2013 High

    Discovery of KDM2B's dual transcriptional role—repressing developmental genes with Polycomb while activating metabolic genes with MYC/KDM5A—in pancreatic cancer established it as a bifunctional chromatin regulator rather than a dedicated repressor.

    Evidence Genome-wide ChIP-seq, gene expression profiling, gain/loss-of-function in mouse PDAC model

    PMID:23321669

    Open questions at the time
    • Structural basis for switching between repressive and activating complexes unknown
    • Whether MYC interaction is direct or chromatin-proximity-mediated
  10. 2015 High

    Complete Fbxl10 inactivation caused de novo DNA methylation specifically at Polycomb/FBXL10-co-occupied promoters, establishing KDM2B as the first factor whose loss causes gain of DNA methylation and revealing an unexpected link between CpG island PRC1 recruitment and DNA methylation protection.

    Evidence Fbxl10 knockout mouse, whole-genome bisulfite sequencing, genetic epistasis with PRC1/PRC2 knockouts

    PMID:25848754

    Open questions at the time
    • Mechanism by which KDM2B/PRC1 prevents DNMT access not elucidated
    • Whether this is a direct or indirect effect of H2AK119ub1 loss
  11. 2016 High

    Crystal structure of the KDM2B/SKP1/BCORL1/PCGF1 tetramer revealed the architectural basis for PRC1.1 assembly, showing that BCORL1 creates a unique extended interface for KDM2B recruitment distinct from other PRC1 variants.

    Evidence Crystal structure determination, in vitro complex assembly, analytical ultracentrifugation

    PMID:27568929

    Open questions at the time
    • No structure of full PRC1.1 with RING1B or DNA/nucleosome substrate
    • How the F-box/LRR region integrates with SCF versus PRC1 architecturally
  12. 2016 High

    Identification of KDM2B as an SCF E3 ubiquitin ligase F-box subunit that targets c-Fos for degradation established a non-chromatin enzymatic function and revealed a phosphorylation-dependent switch controlling substrate release.

    Evidence In vitro ubiquitylation assay, Co-IP, phosphomimetic c-Fos mutants, EGF stimulation

    PMID:26725323

    Open questions at the time
    • Full substrate repertoire of SCF(KDM2B) unknown
    • How cells balance KDM2B between PRC1.1 and SCF complexes
  13. 2016 High

    Comprehensive analysis of Kdm2b-null hematopoietic stem cells revealed context-dependent roles—maintaining lymphoid leukemias but restraining RAS-driven myeloid transformation—demonstrating that KDM2B's function is not uniformly oncogenic or tumor-suppressive.

    Evidence Kdm2b-null mice, RNA-seq, ChIP-seq in human leukemias, HSPC transplantation

    PMID:26808549

    Open questions at the time
    • Molecular basis for cell-type-specific oncogenic versus tumor-suppressive switching not defined
    • Role of specific KDM2B domains in each context not dissected
  14. 2018 High

    Discovery that the FRRUC complex (FBXL10-RNF68-RNF2) is recruited to DNA damage sites via PARP1/TIMELESS to catalyze H2AK119ub1 and promote H2A.Z loading and homologous recombination extended KDM2B's function beyond transcriptional regulation into the DNA damage response.

    Evidence Live-cell imaging at laser-induced damage sites, Co-IP, ChIP, epistasis with canonical PRC1, HR repair assays

    PMID:29985131

    Open questions at the time
    • Structural basis for PARP1/TIMELESS-mediated recruitment unknown
    • Whether FRRUC and PRC1.1 are the same or distinct complexes at damage sites
    • Relative contribution versus canonical PRC1 in DDR
  15. 2018 Medium

    Demonstrating KDM2B demethylase activity toward H3K79me2/me3 expanded its substrate repertoire beyond H3K36/K4 and identified HOXA7/MEIS1 repression as a functional consequence, with implications for leukemia gene regulation.

    Evidence In vitro demethylase assay on H3K79 substrates, genome-wide H3K79me ChIP-seq, SIRT1 displacement analysis

    PMID:29763382

    Open questions at the time
    • H3K79 demethylase activity not independently confirmed by a second lab
    • Relative catalytic efficiency toward H3K79 versus H3K36 not quantified
  16. 2019 High

    KDM2B was shown to activate IL-6 transcription independently of its demethylase activity by recruiting Brg1 (SWI/SNF) and RNA Polymerase II, revealing a scaffolding/transcriptional activation mode distinct from its canonical repressive functions.

    Evidence Co-IP for KDM2B-Brg1, ChIP for Pol II, ATAC-seq, conditional KO mice with endotoxin challenge

    PMID:31197256

    Open questions at the time
    • Whether SWI/SNF cooperation is widespread or locus-specific
    • Structural basis for demethylase-independent activation unclear
  17. 2019 High

    Establishing KDM2B CxxC domain deletion as sufficient to cause NOTCH1-dependent T-ALL in mice demonstrated that PRC1.1-mediated silencing at CpG islands restrains oncogenic signaling and identified a tumor suppressor function.

    Evidence Hematopoietic-specific CxxC domain deletion, genome-wide ChIP-seq for PRC marks, comparison with NOTCH1 targets in human T-ALL

    PMID:31471323

    Open questions at the time
    • Whether pharmacological restoration of PRC1.1 could treat T-ALL
    • Mechanism by which PRC1.1 specifically restrains NOTCH1 targets not fully defined
  18. 2020 Medium

    KDM2B-mediated H3K79 demethylation was linked to PCNA chromatin dissociation during S phase, connecting KDM2B enzymatic activity to DNA replication control beyond transcriptional regulation.

    Evidence PCNA-H3K79me peptide pulldown, ITC binding measurements, iPOND, DNA fiber assay, histone mutant epistasis

    PMID:33029857

    Open questions at the time
    • H3K79 demethylase activity of KDM2B still awaits independent replication
    • In vivo replication phenotype not assessed in animal models
  19. 2021 Medium

    Identification of SRF K165 as a non-histone demethylation target of KDM2B established that its enzymatic activity extends to transcription factor regulation, modulating skeletal muscle differentiation.

    Evidence In vitro demethylation assay on SRF, Co-IP, ChIP for SRF at muscle gene promoters, differentiation assays

    PMID:33564100

    Open questions at the time
    • Full non-histone substrate repertoire unexplored
    • In vivo muscle phenotype in Kdm2b-deficient animals not reported
  20. 2022 High

    CxxC domain-specific knock-in mice showed that impaired PRC1 recruitment in neural stem cells causes senescence, NSC loss, and ASD/ID-like behavioral deficits, directly linking KDM2B-PRC1.1 to neurodevelopmental phenotypes.

    Evidence CxxC domain mutant knock-in mice, ChIP for PRC1/H2AK119ub1, RNA-seq, NSC assays, behavioral phenotyping

    PMID:35128353

    Open questions at the time
    • Whether phenotype is entirely PRC1-dependent or involves demethylase-independent scaffolding
    • Human genetic validation not yet available at this time point
  21. 2023 High

    In vivo CxxC deletion demonstrated KDM2B controls hippocampal neurogenesis by silencing Wnt signaling genes through Polycomb recruitment, causing spatial memory deficits when lost, and multi-omics in cancer cells revealed KDM2B/PRC1.1 regulates amino acid metabolism via MYC/ATF4 co-occupancy.

    Evidence Conditional CxxC deletion mice with behavioral testing and Wnt rescue; multi-omics (RNA-seq, proteomics, metabolomics, ATAC-seq, ChIP-seq) in TNBC cells

    PMID:37838801 PMID:37935302

    Open questions at the time
    • Whether Wnt de-repression is the sole driver of hippocampal defects
    • Generality of metabolic regulation across cancer types
  22. 2025 Medium

    Functional characterization of patient-derived KDM2B CxxC missense variants confirmed that reduced DNA-binding ability is the molecular mechanism underlying a neurodevelopmental syndrome, providing the genotype-to-mechanism link for human disease.

    Evidence In vitro DNA-binding assays with mutant proteins, protein expression assays, episignature analysis in clinical cohort

    PMID:40420380

    Open questions at the time
    • Whether CxxC variants affect PRC1.1 recruitment genome-wide in patient cells not yet shown
    • Therapeutic approaches not explored
    • Independent replication of episignature needed

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: how KDM2B partitions between PRC1.1, SCF, and FRRUC complexes in a single cell; the full non-histone substrate repertoire; the structural basis for switching between repressive and activating transcriptional roles; and whether the H3K79 demethylase activity represents a major or minor catalytic function in vivo.
  • No structural model of full PRC1.1 on chromatin
  • Partitioning between PRC1.1 and SCF complexes not measured
  • H3K79 demethylase activity not independently replicated

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:0042393 histone binding 4 GO:0140110 transcription regulator activity 4 GO:0098772 molecular function regulator activity 2
Localization
GO:0005634 nucleus 4 GO:0005694 chromosome 3 GO:0005730 nucleolus 1
Pathway
R-HSA-4839726 Chromatin organization 8 R-HSA-74160 Gene expression (Transcription) 5 R-HSA-1266738 Developmental Biology 3 R-HSA-162582 Signal Transduction 3 R-HSA-1640170 Cell Cycle 3 R-HSA-392499 Metabolism of proteins 2 R-HSA-73894 DNA Repair 1
Partners
BCORBCORL1BRG1EZH2PCGF1RING1BSIRT1SKP1
Complex memberships
FRRUC (FBXL10-RNF68-RNF2)PRC1.1 (ncPRC1)SCF(KDM2B)/CRL1

Evidence

Reading pass · 45 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2012 KDM2B (FBXL10) specifically recognizes non-methylated CpG islands via its CxxC zinc-finger domain and recruits Polycomb Repressive Complex 1 (PRC1) to these sites, contributing to histone H2A lysine 119 ubiquitylation (H2AK119ub1) and gene repression genome-wide. Genome-wide ChIP-seq, co-immunoprecipitation, biochemical domain analysis, CxxC domain binding assays eLife High 23256043
2013 Fbxl10/KDM2B interacts with Ring1B and Nspc1 (PCGF1), forming a noncanonical PRC1 complex (ncPRC1) required for H2AK119ub1 in mouse ESCs; Fbxl10 depletion causes loss of Ring1B binding to target genes and major loss of H2AK119ub1, and its DNA-binding capability and PRC1 integration are both required for ubiquitylation. Co-immunoprecipitation, genome-wide ChIP-seq, knockdown/rescue with domain mutants, genetic epistasis Molecular cell High 23395003
2013 Kdm2b maintains mESC pluripotency by binding CpG islands via its CxxC-ZF domain and recruiting PRC1 to repress lineage-specific genes; Oct4 and Sox2 directly regulate Kdm2b transcription, defining an Oct4-Sox2-Kdm2b-PRC1-CGI regulatory axis. ChIP, Co-IP, CxxC domain mutants, loss-of-function (knockdown), gene expression analysis Nature cell biology High 23502314
2008 KDM2B (Jhdm1b) is a histone H3 lysine 36 demethylase (H3K36me1/me2) that targets the p15(Ink4b) locus to repress its expression in an enzymatic activity-dependent manner, thereby regulating cell proliferation and cellular senescence. In vitro histone demethylase assay, ChIP, shRNA knockdown with p15Ink4b rescue epistasis, cell proliferation assays Nature structural & molecular biology High 18836456
2007 JHDM1B/KDM2B is a nucleolar protein that binds the transcribed region of ribosomal DNA and represses ribosomal RNA gene transcription through JmjC domain-dependent demethylation of H3K4me3 in the nucleolus. Subcellular fractionation/localization, ChIP on rDNA, RNAi knockdown, in vitro demethylase assay with JmjC domain mutants, cell size/proliferation assays Nature High 17994099
2007 KDM2B (Fbxl10/JHDM1B) forms a novel complex with Ring1B/Rnf2 that also includes BCOR (BcoR), CK2α, Skp1, and Nspc1/PCGF1; this was identified as a distinct ncPRC1-like complex separate from canonical PRC1 and E2F6 complexes. In vivo biotinylation tagging, streptavidin pulldown, mass spectrometry proteomics, iterative complex purification Molecular & cellular proteomics High 17296600
2011 KDM2B (NDY1) synergizes with EZH2 to repress miR-101 by co-binding its promoter; EZH2 binding to the miR-101 promoter depends on KDM2B, but KDM2B binds independently; this axis mediates FGF-2-driven cell proliferation, migration, and angiogenesis downstream of CREB/DYRK1A. ChIP, Co-IP, promoter reporter assays, shRNA knockdown, epistasis experiments, cell proliferation/migration/angiogenesis assays Molecular cell High 21777817
2011 KDM2B/JHDM1b silences p15(Ink4b) through active demethylation of H3K36me2 at the locus; ectopic KDM2B expression is sufficient to transform hematopoietic progenitors, and its depletion in leukemic stem cells impairs self-renewal in vitro and in vivo. Retroviral overexpression, shRNA knockdown, in vitro and in vivo transplantation assays, ChIP for H3K36me2 Blood High 21310926
2009 Ndy1/KDM2B represses the Ink4a/Arf locus by: (1) counteracting senescence-associated down-regulation of EZH2 via JmjC domain-dependent global H3K27me3 upregulation; (2) directly binding the Ink4a/Arf locus to demethylate H3K36me2 and H3K4me3; (3) promoting Bmi1 binding and blocking RNA Pol II recruitment. ChIP, Co-IP (Ndy1-Ezh2 interaction), demethylase assays, MEF immortalization assays, knockdown/overexpression Proceedings of the National Academy of Sciences High 19202064
2016 Crystal structure of the KDM2B/SKP1/BCORL1/PCGF1 tetrameric complex reveals that the BCORL1 PUFD domain positions residues preceding the PCGF1 RAWUL domain to create an extended interface for KDM2B interaction unique to PRC1.1; in vitro assembly identifies the minimal four-component PRC1.1 complex as two heterodimers (KDM2B/SKP1 and BCORL1/PCGF1). Crystal structure determination, in vitro complex assembly, biochemical pulldown assays, analytical ultracentrifugation Structure High 27568929
2015 Complete inactivation of Fbxl10 leads to dense de novo DNA methylation specifically at promoters co-occupied by FBXL10 and Polycomb repressive complexes, establishing FBXL10 as the first factor whose loss causes gain of genomic DNA methylation; this protection requires FBXL10 but not Polycomb components alone. Fbxl10 knockout mouse model, whole-genome bisulfite sequencing/methylation analysis, genetic epistasis with PRC1/PRC2 component knockouts Nature genetics High 25848754
2013 KDM2B drives pancreatic cancer through two distinct transcriptional mechanisms: (1) repression of developmental genes via co-binding with PcG proteins at transcriptional start sites; (2) activation of metabolic genes (protein synthesis, mitochondrial function) via co-binding with MYC and KDM5A. Gain/loss-of-function in cell lines and mouse models, genome-wide ChIP-seq, gene expression profiling, mouse PDAC model (KrasG12D cooperation) Journal of Clinical Investigation High 23321669
2012 Kdm2b promotes iPSC generation by binding to and demethylating H3K36me2 at early responsive gene promoters, enhancing their activation at the beginning of reprogramming; this capacity depends on both demethylase and DNA-binding activities but is largely independent of its anti-senescence role. Retroviral overexpression in reprogramming, domain mutant rescue (demethylase-dead, DNA-binding mutants), ChIP for H3K36me2, gene expression during reprogramming time course Nature cell biology High 22522173
2018 KDM2B is a histone H3K79 di- and trimethyl demethylase that induces transcriptional repression of HOXA7 and MEIS1 via occupancy of their promoters and H3K79 demethylation; KDM2B-knockdown increases global H3K79 methylation; KDM2B loss displaces SIRT1 from chromatin, increasing H4K16 acetylation. In vitro demethylase assay, genome-wide H3K79 methylation analysis (ChIP-seq), KDM2B knockdown stable cell lines, Co-IP for SIRT1 FASEB journal Medium 29763382
2018 The FRRUC complex (FBXL10-RNF68-RNF2) is rapidly and transiently recruited to DNA damage sites in a PARP1- and TIMELESS-dependent manner, where it promotes H2AK119 mono-ubiquitylation, local H2A.Z incorporation, transcriptional repression, DSB signaling, and homologous recombination repair. Live-cell imaging at laser-induced DNA damage sites, Co-IP, ChIP, genetic knockdowns, epistasis with BMI1-RNF2 and MEL18-RNF2 complexes, HR repair assays eLife High 29985131
2018 In synovial sarcoma, SS18-SSX1 oncoprotein physically interacts with PRC1.1 and co-associates with SWI/SNF and KDM2B on unmethylated CpG islands; via KDM2B, SS18-SSX1 aberrantly activates developmental genes normally silenced by polycomb; KDM2B depletion restores repression and causes irreversible mesenchymal differentiation. Co-IP, ChIP-seq, functional genomics screen, loss-of-function differentiation assays Cancer cell High 29502955
2011 KDM2B counteracts senescence-associated downregulation of EZH2 by silencing let-7b and miR-101 via locus-specific H3K36me2 demethylation at their genomic loci, thereby maintaining EZH2 levels and promoting cellular proliferation/immortalization. Retroviral overexpression, ChIP for H3K36me2 at miRNA loci, let-7b overexpression epistasis, KDM2B knockdown in multiple primary cell types Journal of biological chemistry High 21757686
2007 Fbl10/KDM2B interacts with c-Jun and represses c-Jun-mediated transcription; KDM2B binds unmethylated CpG sequences in the c-jun promoter via its CxxC zinc finger, tethers transcriptional repressor complexes, and requires c-Jun for its promoter recruitment; KDM2B protein is down-regulated in response to UV inversely correlating with c-Jun induction. Co-IP, ChIP, siRNA knockdown, luciferase reporter assays, UV treatment experiments Nature cell biology High 17704768
2016 KDM2B, via its F-box domain, functions as a substrate recognition subunit of the SCF(KDM2B)/CRL1 E3 ubiquitin ligase complex to target c-Fos for polyubiquitylation and degradation; EGF-induced c-Fos S374 phosphorylation dissociates c-Fos from KDM2B, stabilizing c-Fos and enabling cell proliferation. Co-IP, in vitro ubiquitylation assay, phosphomimetic/non-phosphorylatable c-Fos mutants, EGF stimulation experiments, tumor-derived KDM2B mutation analysis Oncogene High 26725323
2014 NDY1/KDM2B functions as a master regulator of PRC1 and PRC2 by silencing a set of miRNAs that target multiple polycomb complex members; NDY1 knockdown de-represses these miRNAs and down-regulates their polycomb targets, reducing cancer stem cell self-renewal and sphere formation. shRNA knockdown in multiple tumor cell lines, mammosphere assays, stem cell marker analysis (ALDH, CD44/CD24), miRNA profiling, epistasis (miRNA re-expression) Cancer research Medium 24853546
2011 Fbxl10/KDM2B deficiency in mouse neural progenitor cells causes increased apoptosis, upregulation of p19ARF (an apoptosis inducer), increased neural progenitor mitosis, and neural tube closure failure leading to exencephaly. Fbxl10 knockout mouse generation, in situ hybridization, TUNEL assay, mitotic cell counting, p19ARF qRT-PCR in embryos and MEFs Molecular and cellular neurosciences Medium 21220025
2019 KDM2B promotes IL-6 production in macrophages independently of its demethylase activity by interacting with Brg1 (SWI/SNF ATPase subunit) to facilitate chromatin accessibility at the Il6 promoter and directly recruiting RNA Polymerase II; KDM2B-deficient mice show decreased IL-6 and resistance to endotoxin shock. Co-IP (KDM2B-Brg1 interaction), ChIP for chromatin accessibility and Pol II, KDM2B conditional KO mice, ELISA for IL-6, ATAC-seq Cellular & molecular immunology High 31197256
2014 FBXL10/KDM2B recruits a noncanonical PRC1 complex containing RING1B, SKP1, PCGF1, and BCOR to specific genomic loci (including Cdk1, Pparg1/2) to repress adipogenesis; this function requires the F-box and leucine-rich repeat domains but not the JmjC demethylase domain. ChIP-seq, Co-IP, domain deletion mutants, siRNA knockdown of RING1B/SKP1, 3T3-L1 differentiation assays Journal of biological chemistry High 25533466
2016 KDM2B cooperates with polycomb and trithorax complexes to regulate hematopoietic stem and progenitor cell differentiation, lineage choice, cytokine signaling, and cell cycle; KDM2B has a dichotomous role—maintaining lymphoid leukemias but restraining RAS-driven myeloid transformation—depending on cellular context. Kdm2b-null mice, RNA-seq, ChIP-seq in human leukemias, HSPC transplantation assays Journal of Clinical Investigation High 26808549
2017 KDM2B regulates somatic reprogramming through PRC1.1 recruitment to CpG islands; BMP-SMAD signaling attenuates PRC1.1 occupancy and H2AK119 ubiquitylation at developmental gene loci, activating mesendodermal factors and suppressing reprogramming. ChIP for PRC1.1 components and H2AK119ub1, BMP4 treatment epistasis, reprogramming efficiency assays with domain mutants Cell reports Medium 29166607
2019 KDM2B in PRC1.1 acts as a tumor suppressor in T-cell leukemogenesis by binding nonmethylated CpG island promoters via its CxxC domain and restricting excessive NOTCH1-mediated transcriptional activation via H2AK119ub1 deposition; Kdm2b-deficient mice develop NOTCH1-dependent T-ALL. Hematopoietic-specific CxxC domain deletion mice, ChIP-seq (KDM2B, BCOR, EZH2, H2AK119ub1, H3K4me3, H3K27me3), comparison with NOTCH1 target genes in human T-ALL Blood advances High 31471323
2021 KDM2B demethylates serum response factor (SRF) at K165 (non-histone target) to negatively regulate skeletal muscle differentiation; SET7 counteracts this by methylating SRF K165; SRF K165 methylation is required for transcriptional activation of SRF-dependent muscle genes and promoter occupancy. Co-IP (KDM2B-SRF interaction), in vitro demethylation assay on SRF, SET7 inhibitor treatment, ChIP for SRF at target promoters, gain/loss-of-function differentiation assays Experimental & molecular medicine Medium 33564100
2018 KDM2B mediates H2AK119 monoubiquitylation as a PRC1 component by recognizing regulatory regions of CDH1, miR200a, and CGN genes via its DNA-recognition property (not demethylase activity), inducing H2AK119ub1 and subsequent EZH2 recruitment and H3K27 methylation required for EMT-related gene repression during TGF-β-induced EMT. ChIP for H2AK119ub1 and H3K27me3, KDM2B domain mutants (DNA-binding vs. demethylase), knockdown/overexpression in lung/pancreatic cancer lines, TGF-β treatment Journal of biological chemistry Medium 33779563
2019 ELKS1 stabilizes KDM2B protein in mast cells, and KDM2B is an essential transcriptional regulator of Syntaxin 4 (STX4) and Stxbp2 expression required for mast cell degranulation. Mast cell-specific Elks1 conditional KO mice, Co-IP (ELKS1-KDM2B interaction), ChIP for KDM2B at Stx4/Stxbp2 promoters, degranulation assays in vitro and in vivo Science advances Medium 32937583
2020 KDM2B-mediated H3K79 demethylation facilitates PCNA dissociation from chromatin during S phase by abolishing H3K79me-dependent PCNA chromatin binding; KDM2B depletion causes aberrant PCNA retention on chromatin and impairs DNA replication efficiency. PCNA-H3K79me peptide pulldown, isothermal titration calorimetry (ITC), ChIP, iPOND, DNA fiber assay, flow cytometry, KDM2B-depleted cells and H3K79R histone mutants Cell proliferation Medium 33029857
2019 Tip60 acetyltransferase acetylates KDM2B at lysine 758, which decreases KDM2B's ability to bind nucleosomes and reduces its demethylase activity toward nucleosomal (but not bulk) histone substrates, diminishing KDM2B occupancy at p21 and puma promoters and promoting tumor growth. Co-IP, in vitro acetylation/demethylase assays with nucleosome vs. bulk histone substrates, K758 acetylation mutants, ChIP for KDM2B binding, tumor xenograft models Journal of cellular and molecular medicine Medium 31218831
2021 FBXL10/KDM2B stabilizes ERRα protein by reducing its polyubiquitylation and promoting its mono-ubiquitylation, thereby increasing ERRα transcriptional activity and promoter occupancy at ERRα target genes to facilitate breast cancer cell proliferation. Co-IP (mass spectrometry identification then validated), ubiquitylation assays (poly vs. mono-Ub), reporter gene assay, ChIP for ERRα, in vitro and in vivo proliferation/tumor assays Cancer letters Medium 33450359
2021 FBXL10/KDM2B promotes EMT and breast cancer metastasis by interacting with SNAI1 and facilitating SNAI1-HDAC1 interaction, resulting in SNAI1 deacetylation and enhanced transcriptional repression of CDH1/E-cadherin. Co-IP (FBXL10-SNAI1-HDAC1 ternary complex), reporter assays for CDH1 transcription, E-cadherin protein level measurements, lung metastasis mouse model Cell death discovery Medium 34718323
2020 Alternative short isoforms of KDM2B (KDM2B-SF), lacking the N-terminal demethylase domain but retaining CxxC and other domains, negatively regulate canonical Wnt signaling by binding Axin2 and cyclin D1 promoters and interacting with TCF7L1, repressing Wnt target gene transcription in a DNA-binding domain-dependent manner. Luciferase reporter assays (Wnt-responsive element), ChIP, Co-IP with TCF7L1, domain deletion mutant analysis PloS one Medium 33104714
2023 KDM2B controls hippocampal morphogenesis and neurogenesis by transcriptionally silencing Wnt signaling genes in neural progenitors through CxxC domain-dependent chromatin association and recruitment of Polycomb repressive complexes; loss of CxxC domain (Kdm2b∆CxxC mice) causes de-repression of Wnt genes, impaired neural progenitor migration/differentiation, and spatial memory deficits. Conditional CxxC domain deletion mice, ChIP for PRC marks, RNA-seq, behavioral testing (spatial memory, fear conditioning), lineage tracing, Wnt pathway activation rescue experiments Nature communications High 37838801
2022 Loss of KDM2B CxxC-ZF domain impairs PRC1 recruitment to chromatin in neural stem cells (NSCs), causing de-repression of apoptosis and cell-cycle arrest genes, NSC senescence, loss of NSC populations in mouse brain, and ASD/ID-like behavioral and memory deficits. CxxC domain mutant knock-in mice, ChIP for PRC1/H2AK119ub1, RNA-seq, NSC culture assays, behavioral phenotyping iScience High 35128353
2018 EBNA3C (EBV nuclear antigen) interacts with KDM2B, and this interaction is required for H3K4me3 removal at EBNA3C target gene promoters (COBLL1, ADAM28-ADAMDEC1 locus) and for full EBNA3C-mediated transcriptional repression in lymphoblastoid cells. Co-IP (EBNA3C-KDM2B), ChIP for H3K4me3 at target loci, recombinant EBV with EBNA3C RBPJ-motif mutants, gene expression analysis Journal of virology Medium 30135119
2019 KDM2B represses Choline Kinase α (CKα) expression by binding to its promoter (Box2) during neuroblast proliferation, maintaining the undifferentiated state; KDM2B knockdown enhances CKα expression and induces neuronal differentiation even without retinoic acid. ChIP (KDM2B at Chka promoter), siRNA knockdown, gain-of-function, retinoic acid differentiation assays PloS one Medium 30629659
2023 KDM2B, functioning in the ncPRC1.1 context, regulates amino acid metabolism (SGOC, glutamate, GSH pathways) by enhancing chromatin accessibility and expression of MYC and ATF4, with KDM2B co-occupying promoters of metabolic genes together with MYC and ATF4. Multi-omics (RNA-seq, quantitative TMT proteomics, metabolomics, ATAC-seq, ChIP-seq), shRNA knockdown in TNBC cell lines Metabolism Medium 37935302
2016 FBXL10 maintains silencing of DUSP6 (a phosphatase for ERK1/2) via recruitment of Polycomb group proteins and deposition of repressive histone modifications at the DUSP6 promoter, thereby maintaining ERK1/2 phosphorylation and promoting DLBCL cell proliferation. ChIP for PcG marks at DUSP6 promoter, RNA-seq, DUSP6 knockdown rescue of FBXL10-depleted cells, xenograft tumor model Cell death & disease Medium 29352142
2020 KDM2B directly binds the MOB1 promoter and suppresses its transcriptional activity, thereby regulating the Hippo pathway; KDM2B promotes PDAC proliferation, migration, and invasion via MOB1 suppression. ChIP for KDM2B at MOB1 promoter, promoter luciferase assay, gain/loss-of-function with MOB1 epistasis Journal of experimental & clinical cancer research Medium 31941533
2019 LncKdm2b (Kancr), divergently transcribed from a bidirectional promoter of Kdm2b, positively regulates Kdm2b transcription in cis by associating with hnRNPAB to facilitate a permissive chromatin environment at the Kdm2b promoter; LncKdm2b and Kdm2b are both required for proper differentiation and migration of cortical projection neurons. In vivo lineage tracing, phenotypic analysis, RNA-protein interaction (hnRNPAB pulldown), chromatin accessibility assays, CRISPRi knockdown Protein & cell Medium 31317506
2023 DHX9 helicase enhances H3K9 chromatin demethylation by KDM2B at the YAP1 promoter and facilitates RNA Polymerase II recruitment, promoting YAP1 expression in Ewing sarcoma; DHX9 and KDM2B form a functional complex, and this axis is counteracted by EWS-FLI1 binding to the YAP1 promoter. Co-IP (DHX9-KDM2B), ChIP for H3K9me and Pol II at YAP1 promoter, transcriptome profiling, functional transformation assays Oncogene Medium 38017132
2021 KDM2B inactivation via CRISPR-Cas9 genome-wide screen suppresses multiple heparan sulfate (HS) sulfotransferases and upregulates SULF1 sulfatase, altering HS structure and protein binding; KDM2B-deficient cell growth defects are rescued by SULF1 inactivation, establishing KDM2B as a master regulator of extracellular matrix gene expression. Genome-wide CRISPR-Cas9 screen, RNA-seq, HS sulfotransferase activity assays, SULF1 genetic epistasis Nature chemical biology Medium 33846619
2025 KDM2B CxxC domain missense variants significantly reduce its DNA-binding ability (measured functionally in vitro) while allowing protein expression; this DNA-binding impairment is the molecular mechanism distinguishing CxxC variants from haploinsufficiency variants, associated with a distinct neurodevelopmental syndrome phenotype. Functional DNA-binding assays with mutant KDM2B proteins, protein expression assays in vitro, clinical cohort correlation with episignature analysis Human molecular genetics Medium 40420380

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 367 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 252 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
2011 FGF-2 regulates cell proliferation, migration, and angiogenesis through an NDY1/KDM2B-miR-101-EZH2 pathway. Molecular cell 183 21777817
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 183 17296600
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 145 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 118 25848754
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
2018 The SS18-SSX Oncoprotein Hijacks KDM2B-PRC1.1 to Drive Synovial Sarcoma. Cancer cell 105 29502955
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 102 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 77 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 The critical role of histone lysine demethylase KDM2B in cancer. American journal of translational research 60 30210666
2018 HPV16 E6 and E7 upregulate the histone lysine demethylase KDM2B through the c-MYC/miR-146a-5p axys. Oncogene 59 29335520
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) 49 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 43 31216469
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 KDM2B/FBXL10 targets c-Fos for ubiquitylation and degradation in response to mitogenic stimulation. Oncogene 40 26725323
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 34 31317506
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, an H3K36-specific demethylase, regulates apoptotic response of GBM cells to TRAIL. Cell death & disease 33 28661478
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
2017 Kdm2b Regulates Somatic Reprogramming through Variant PRC1 Complex-Dependent Function. Cell reports 32 29166607
2013 Knockdown of fbxl10/kdm2bb rescues chd7 morphant phenotype in a zebrafish model of CHARGE syndrome. Developmental biology 32 23920116
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
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
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 19 28415746
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 17 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
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 KDM2B regulates hippocampal morphogenesis by transcriptionally silencing Wnt signaling in neural progenitors. Nature communications 11 37838801
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 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 10 37935302
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
2016 Enhanced direct conversion of fibroblasts into hepatocyte-like cells by Kdm2b. Biochemical and biophysical research communications 10 27103435
2023 KDM2B regulates inflammation and oxidative stress of sepsis via targeting NF-κB and AP-1 pathways. Immunity, inflammation and disease 9 37773725
2022 Impaired KDM2B-mediated PRC1 recruitment to chromatin causes defective neural stem cell self-renewal and ASD/ID-like behaviors. iScience 9 35128353
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 9 35580699
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
2019 KDM2B regulates choline kinase expression and neuronal differentiation of neuroblastoma cells. PloS one 9 30629659
2019 Induction of co-inhibitory molecule CTLA-4 by human papillomavirus E7 protein through downregulation of histone methyltransferase JHDM1B expression. Virology 9 31590057
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
2024 KDM2B regulates stroke injury by modulating OGT-mediated 0-GlcNAcylation of SLC7A11. Communications biology 8 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 8 37634866
2020 KDM2B-associated paunch calf syndrome in Marchigiana cattle. Journal of veterinary internal medicine 7 32515858
2023 The DNA/RNA helicase DHX9 orchestrates the KDM2B-mediated transcriptional regulation of YAP1 in Ewing sarcoma. Oncogene 6 38017132
2025 SAMD4A inhibits abdominal aortic aneurysm development and VSMC phenotypic transformation through targeting KDM2B. Journal of advanced research 5 40081568
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
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
2021 Oncogenic role of ALX3 in cervical cancer cells through KDM2B-mediated histone demethylation of CDC25A. BMC cancer 5 34266408
2016 Overexpression of histone demethylase Fbxl10 leads to enhanced migration in mouse embryonic fibroblasts. Experimental cell research 5 27646113
2024 KDM2B and its peptides promote the stem cells from apical papilla mediated nerve injury repair in rats by intervening EZH2 function. Cell proliferation 4 39358887
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