Affinage

KDM2A

Lysine-specific demethylase 2A · UniProt Q9Y2K7

Length
1162 aa
Mass
132.8 kDa
Annotated
2026-06-10
93 papers in source corpus 40 papers cited in narrative 41 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 9/9 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

KDM2A is a JmjC-domain histone demethylase that selectively removes mono- and di-methyl marks from histone H3 lysine 36 (H3K36me1/me2), with H3K36me3 normally excluded by steric constraints on substrate rearrangement in the catalytic groove (PMID:20379134, PMID:25128496, PMID:24553073, PMID:38781256). Genome-wide targeting is achieved through its ZF-CXXC domain, which reads non-methylated CpG dinucleotides on linker DNA and recognizes CpG islands by combining unmethylated DNA state with reduced nucleosome occlusion; productive nucleosome engagement additionally depends on the acidic patch and DNA unwrapping (PMID:36797403, PMID:22083960, PMID:39522683). Together with KDM2B, KDM2A protects CpG islands from aberrant DNA methylation in a catalysis-dependent manner (PMID:39522683), and it integrates heterochromatin signals by binding HP1 through an LxVxL motif, coupling H3K9me3-marked chromatin to its demethylase function (PMID:28180290, PMID:19001877). At rDNA promoters KDM2A localizes to nucleoli and represses rRNA transcription by demethylating H3K36me2 in response to energy deprivation, an activity stimulated by AMPK signaling and by reduction of intracellular succinate following glucose starvation or metformin, and modulated by Ser731 phosphorylation that governs PHF8 binding (PMID:20379134, PMID:26416883, PMID:31822720, PMID:40427554). KDM2A participates in the DNA double-strand break response: ATM phosphorylates it at T632 and SIRT6 mono-ADP-ribosylates it, both displacing KDM2A from chromatin to raise local H3K36me2 that recruits the MRE11/NBS1 complex and NHEJ machinery (PMID:25823024, PMID:32584788). Beyond demethylation, KDM2A functions through its F-box/CXXC-dependent activities to direct ubiquitin- and neddylation-coupled degradation of nuclear non-phosphorylated β-catenin, PFKFB3, and TCF/LEF factors (PMID:26004508, PMID:37998355, PMID:34079757). In oncogenic contexts KDM2A silences tumor-suppressor loci including DUSP3, HDAC3, and TET2 via H3K36me2 demethylation (PMID:24200691, PMID:24482232, PMID:28785073), antagonizes NSD1-dependent H3K36me2 writing to suppress T-cell chemokine expression (PMID:37311054), and promotes de-clustering of ALT telomeres via SENP6-mediated SUMO deconjugation (PMID:36991019). In vivo, KDM2A is essential for embryogenesis (PMID:25463925) and shapes cell fate across tissues, restraining macrophage M2 polarization at the Pparg locus, controlling slow-twitch myofiber identity through Esrrg splicing, and governing meiotic gene programs in male germ cells (PMID:33462408, PMID:39160277, PMID:39870955). De novo KDM2A variants cause intellectual disability through altered protein stability and localization (PMID:41468891, PMID:38060137).

Mechanistic history

Synthesis pass · year-by-year structured walk · 28 steps
  1. 2007 High

    Established the founding biochemical identity of KDM2A by showing it is an enzyme that erases a specific histone mark, defining its molecular activity.

    Evidence In vitro demethylase assays and mass spectrometry of histone modifications

    PMID:20379134 PMID:24553073 PMID:25128496

    Open questions at the time
    • Did not explain the structural basis of H3K36me1/2 selectivity versus me3 exclusion
    • Genomic targeting mechanism not yet addressed
  2. 2014 High

    Resolved how KDM2A discriminates methylation states, showing substrate threading and active-site geometry enforce H3K36me1/me2 specificity and exclude me3.

    Evidence X-ray crystallography with structure-guided mutagenesis and cancer-phenotype functional assays

    PMID:25128496

    Open questions at the time
    • Did not capture KDM2A engaging an intact nucleosome
    • Catalytic chemistry of the off-line-to-in-line transition not directly observed
  3. 2024 Medium

    Defined the catalytic chemistry of state selectivity, identifying Y222 conformational control of 2-oxoglutarate rearrangement as the basis for H3K36me3 inactivity.

    Evidence QM/MM and molecular dynamics simulations with variant analysis

    PMID:38781256

    Open questions at the time
    • Computational only; no experimental wet-lab Y222 mutagenesis validation reported
    • Relevance of predicted variants to cellular activity untested
  4. 2023 High

    Revealed how KDM2A reaches its substrate on chromatin, showing nucleosome binding requires the acidic patch and DNA unwrapping — distinguishing it from KDM2B.

    Evidence Cryo-EM of KDM2A trapped on nucleosomes via a covalent H3K36-inhibitor conjugate plus acidic-patch interactome screen

    PMID:36797403

    Open questions at the time
    • Did not address regulation of nucleosome engagement in vivo
    • Interplay with CpG-island targeting not resolved structurally
  5. 2011 High

    Identified the genomic targeting principle, showing the ZF-CXXC domain recruits KDM2A to unmethylated CpG islands via linker DNA with nucleosomes as a barrier.

    Evidence Defined chromatin templates in vitro combined with in vivo chromatin profiling and ZF-CXXC biochemistry

    PMID:22083960

    Open questions at the time
    • Did not establish functional consequence of CGI binding genome-wide
    • Did not separate targeting from catalytic requirement
  6. 2010 High

    Connected KDM2A catalysis to nucleolar rRNA control and metabolic state, showing it represses rRNA transcription under starvation and is inhibited by succinate.

    Evidence Overexpression/knockdown, ChIP, nucleolar microscopy, and succinate inhibition at the rDNA promoter

    PMID:20379134

    Open questions at the time
    • Upstream signaling linking starvation to KDM2A activity not defined
    • Did not separate CpG-binding from catalytic requirement at rDNA
  7. 2015 High

    Mapped the energy-sensing pathway, showing AMPK signaling and CxxC-ZF-dependent rDNA binding are both required for starvation-induced rRNA repression.

    Evidence 2-DG/AMPK inhibition with domain mutagenesis, ChIP, and knockdown-rescue in breast cancer cells

    PMID:24553073 PMID:26416883

    Open questions at the time
    • Did not resolve how AMPK mechanistically modifies KDM2A
    • Succinate contribution not yet separated from AMPK
  8. 2019 Medium

    Dissected the dual metabolic inputs, showing metformin activates KDM2A only when AMPK activation is combined with succinate reduction.

    Evidence Metformin treatment with metabolite supplementation, AMPK inhibition, and ChIP

    PMID:31822720

    Open questions at the time
    • Direct molecular target of AMPK on KDM2A not identified here
    • Single-lab pharmacological dissection
  9. 2025 Medium

    Identified a phospho-switch regulating rDNA activity, showing AMPK-driven Ser731 dephosphorylation reduces inhibitory PHF8 binding to activate KDM2A.

    Evidence Co-IP, domain mapping, S731A mutagenesis, and rRNA transcription assays

    PMID:40427554

    Open questions at the time
    • Direct kinase/phosphatase acting on Ser731 not fully defined
    • Single-lab finding awaiting independent confirmation
  10. 2008 Medium

    Linked KDM2A to heterochromatin maintenance, showing it interacts with HP1, associates with centromeres, and represses satellite RNA transcription.

    Evidence siRNA knockdown, epigenetic reporter, co-IP, centromere ChIP/IF, and satellite-RNA overexpression

    PMID:19001877

    Open questions at the time
    • The HP1-binding motif was not mapped here
    • Causal direction between HP1 localization and heterochromatin state incompletely resolved
  11. 2017 High

    Defined the molecular HP1 interface, mapping an LxVxL-type motif that couples DNA methylation and H3K9me3 signals through a multivalent nucleosome module.

    Evidence Biochemical pulldown, direct binding assays, motif mutagenesis, and in vivo zebrafish assay

    PMID:28180290

    Open questions at the time
    • Did not establish which HP1 paralog dominates in vivo
    • Functional output of HP1 coupling at native loci not fully resolved
  12. 2019 Medium

    Connected HP1 binding to nucleolar function, showing HP1γ binding at V801 is required for nucleolar accumulation and starvation-induced rRNA repression.

    Evidence Co-IP, V801 point mutagenesis, HP1γ knockdown, and nucleolar microscopy/ChIP

    PMID:31413816

    Open questions at the time
    • Mechanism linking HP1γ to nucleolar retention not detailed
    • Single-lab finding
  13. 2015 High

    Established KDM2A's role in the DSB response, showing ATM-mediated T632 phosphorylation displaces it from chromatin, raising H3K36me2 to recruit MRE11/NBS1.

    Evidence Co-IP, ATM interaction, T632 mutagenesis/mass spectrometry, ChIP, and DNA-damage repair assays

    PMID:25823024

    Open questions at the time
    • How elevated H3K36me2 is specifically read by NBS1 at damage sites not fully resolved
    • Kinetics of re-loading after repair unaddressed
  14. 2020 Medium

    Added a second displacement mechanism, showing SIRT6 mono-ADP-ribosylates KDM2A to elevate H3K36me2, drive H3K9me3/HP1α, and recruit NHEJ factors.

    Evidence SIRT6 enzymatic assay, chromatin displacement, H3K36me2/H3K9me3 ChIP, and NHEJ recruitment assays

    PMID:32584788

    Open questions at the time
    • ADP-ribosylation site on KDM2A not defined
    • Relationship between SIRT6 and ATM-driven displacement not reconciled
  15. 2015 High

    Revealed a non-histone catalytic axis, showing KDM2A demethylates and then ubiquitylates nuclear non-phosphorylated β-catenin to control Wnt signaling.

    Evidence Domain-mapped interaction assays, coupled methylation-ubiquitylation assays, and Xenopus embryo knockdown

    PMID:26004508

    Open questions at the time
    • The methyltransferase generating the β-catenin methyl mark not identified
    • Demethylase-versus-F-box contributions not fully partitioned
  16. 2023 Medium

    Extended demethylase-independent degradation activity, showing CXXC- and neddylation-dependent KDM2A degrades TCF/LEF factors including TCF7L2.

    Evidence Co-IP, domain deletion, proteasome and neddylation inhibition, and stability assays

    PMID:33104714 PMID:37998355

    Open questions at the time
    • E3 complex composition not biochemically reconstituted
    • In vivo relevance of TCF/LEF turnover untested
  17. 2021 Medium

    Generalized the E3 ligase function to metabolism, showing F-box-dependent KDM2A ubiquitylates PFKFB3 to suppress myeloma proliferation independent of demethylase activity.

    Evidence Co-IP, ubiquitylation and stability assays in myeloma cells

    PMID:34079757

    Open questions at the time
    • SCF complex assembly not directly demonstrated
    • Single-lab finding
  18. 2013 High

    Defined oncogenic gene silencing, showing KDM2A demethylates H3K36me2 to repress DUSP3 and thereby activate ERK1/2 signaling in NSCLC.

    Evidence Catalytic mutant comparison, ChIP at DUSP3, ERK1/2 phosphorylation, and rescue assays

    PMID:24200691

    Open questions at the time
    • Did not address breadth of repressed loci genome-wide
    • Selectivity of locus targeting not explained
  19. 2014 High

    Extended the silencing program, showing KDM2A represses HDAC3 to de-repress CDK6/NANOS1 and promote NSCLC tumorigenicity, and physically engages Rb/E2F1 to control proliferative promoters.

    Evidence Catalytic-mutant knockdown/overexpression, ChIP, double-knockdown rescue, xenografts, and cell-cycle-synchronized Co-IP

    PMID:24482232 PMID:25029110

    Open questions at the time
    • Mechanism directing KDM2A to specific repressive targets unresolved
    • E2F1 regulation mechanism only partly defined
  20. 2017 Medium

    Linked KDM2A to DNA hydroxymethylation control, showing KDM2A co-occupies the TET2 promoter with RelA to repress TET2 and promote breast cancer invasion.

    Evidence Co-IP, ChIP, knockdown-rescue, 5-hmC measurement, and invasion assays

    PMID:28785073

    Open questions at the time
    • Whether repression requires demethylase activity not fully resolved
    • Single-lab finding
  21. 2023 High

    Identified a unique telomere maintenance role, showing KDM2A enables SENP6-mediated SUMO deconjugation to de-cluster ALT telomeres and preserve chromosome segregation.

    Evidence CRISPR screens, KDM2A/SENP6 epistasis, telomere SUMO assays, and segregation analysis

    PMID:36991019

    Open questions at the time
    • Molecular link between KDM2A and SENP6 activity not defined
    • Whether this requires demethylase or F-box activity unresolved
  22. 2014 High

    Established organismal essentiality, showing Fbxl11/Kdm2a knockout is embryonic lethal with reduced Ezh2/H2Aub and elevated p21.

    Evidence Knockout mouse generation with histology and molecular profiling

    PMID:25463925

    Open questions at the time
    • Causal chain from KDM2A loss to Ezh2 reduction not mechanistically defined
    • Tissue-specific contributions not separated
  23. 2016 Medium

    Defined a stem/progenitor differentiation role, showing KDM2A with co-factor BCOR represses cell-cycle inhibitors, stemness genes, and differentiation regulators in SCAPs.

    Evidence shRNA knockdown of KDM2A and BCOR, ChIP for H3K4me3/H3K36me, and differentiation assays

    PMID:23559091 PMID:23872478 PMID:27074224

    Open questions at the time
    • Relationship between H3K4me3 changes and KDM2A's H3K36me2 catalysis unclear
    • BCOR-KDM2A complex not biochemically reconstituted
  24. 2021 High

    Linked KDM2A catalysis to immunometabolic cell fate, showing myeloid Kdm2a loss raises H3K36me2 at Pparg to drive M2 polarization and protect against obesity.

    Evidence Conditional KO with Pparg H3K36me2 ChIP, ATAC-seq, Stat6 ChIP, and metabolic phenotyping

    PMID:33462408

    Open questions at the time
    • Did not establish direct KDM2A recruitment mechanism to Pparg
    • Demethylase-versus-other-activity contribution not isolated
  25. 2024 High

    Defined germline and CpG-island roles, showing KDM2A balances H3K36me2/3, recruits E2F1/HCFC1 to meiotic genes, and (with KDM2B) protects CpG islands from DNA methylation through catalysis.

    Evidence Conditional KO mice with ChIP-seq/Co-IP, plus Kdm2a/2b single/double KO and JmjC catalytic mutants with methylation profiling

    PMID:39160277 PMID:39522683 PMID:40701999

    Open questions at the time
    • The reported H3K36me3 activity in germ cells differs from the canonical me1/2 specificity and is not structurally explained
    • Polycomb coupling mechanism at CpG islands not fully defined
  26. 2025 High

    Extended catalytic control to muscle metabolism, showing Kdm2a loss raises H3K36me2 at Esrrg to recruit Mrg15 for splicing and drive slow-twitch transition.

    Evidence Muscle-specific conditional KO with Esrrg H3K36me2 ChIP, Mrg15 co-IP/ChIP, splicing analysis, and metabolic phenotyping

    PMID:39870955

    Open questions at the time
    • How H3K36me2 mechanistically recruits Mrg15 to splicing not fully resolved
    • Direct KDM2A targeting to Esrrg not mapped
  27. 2023 Medium

    Defined immune-evasion and regulatory contexts, showing KDM2A antagonizes NSD1 H3K36me2 writing to suppress chemokine expression and is itself stabilized or transcriptionally induced in tumor microenvironments.

    Evidence KDM2A knockdown with ChIP and immunocompetent/immunodeficient tumor models; Co-IP/ChIP for SYVN1-RANGAP1 stability and STAT3/NFκB p50 promoter regulation

    PMID:37311054 PMID:37821959 PMID:37845585 PMID:38451221

    Open questions at the time
    • Stability and transcriptional findings rest largely on single-lab Co-IP/ChIP
    • Whether chemokine repression is purely catalytic not fully isolated
  28. 2025 Medium

    Connected KDM2A to human disease, showing de novo variants cause intellectual disability via altered stability, localization, and impaired regulation of neurodevelopmental gene programs.

    Evidence Human cell variant localization/stability assays, Drosophila epistasis, and ChIP-seq/RNA-seq in neural models

    PMID:38060137 PMID:41468891

    Open questions at the time
    • Loss- versus gain-of-function contributions differ across variants and are not fully reconciled
    • Mechanism connecting MAPK-locus H3K36me2 to neuronal phenotype incomplete

Open questions

Synthesis pass · forward-looking unresolved questions
  • How KDM2A's distinct activities — H3K36me2 demethylase, CpG-island reader, and F-box/SCF ubiquitin ligase — are partitioned, coordinated, and selectively deployed at specific loci and substrates in vivo remains unresolved.
  • No unified model partitioning catalytic versus ligase functions across contexts
  • Mechanism selecting specific repressive target loci genome-wide undefined
  • Reported H3K36me3 activity conflicts with canonical me1/2 specificity

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140098 catalytic activity, acting on RNA 4 GO:0140110 transcription regulator activity 4 GO:0003677 DNA binding 3 GO:0016491 oxidoreductase activity 3 GO:0140096 catalytic activity, acting on a protein 3 GO:0016874 ligase activity 2
Localization
GO:0000228 nuclear chromosome 3 GO:0005634 nucleus 3 GO:0005730 nucleolus 3
Pathway
R-HSA-74160 Gene expression (Transcription) 4 R-HSA-1266738 Developmental Biology 3 R-HSA-392499 Metabolism of proteins 3 R-HSA-4839726 Chromatin organization 3 R-HSA-162582 Signal Transduction 2 R-HSA-73894 DNA Repair 2
Partners
ATMCTNNB1E2F1HP1NBS1PHF8SIRT6TCF7L2
Complex memberships
KDM2A/B-PRC1SCF (F-box) ubiquitin ligase

Evidence

Reading pass · 41 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2007 KDM2A (JHDM1A/FBXL11) is a JmjC-domain-containing histone demethylase that specifically demethylates mono- and dimethylated histone H3 lysine 36 (H3K36me1/me2), with little or no activity on trimethylated H3K36. In vitro demethylase assays, mass spectrometry of histone modifications Multiple papers (e.g., Molecular and cellular biology, EMBO journal) High 20379134 24553073 25128496
2014 Structural studies revealed that H3K36 specificity for KDM2A is mediated by U-shaped threading of the H3K36 peptide through a catalytic groove; key residues G33, G34 (positioned in a narrow channel), P38 (turn residue), and Y41 (inserts into its own pocket) contribute to K36me specificity. Steric constraints prevent trimethylated K36 from undergoing the 'off-line'-to-'in-line' transition required for demethylation. Structure-guided active-site mutations abrogated KDM2A-mediated suppression of cancer cell phenotypes. X-ray crystallography, structure-guided mutagenesis, functional assays Genes & development High 25128496
2024 QM/MM and MD simulations demonstrated that KDM2A catalysis is controlled by a conformational change of the second coordination sphere residue Y222, which unlocks 2-oxoglutarate rearrangement from off-line to in-line mode; Y222A variant makes the rearrangement more favorable. The trimethylated lysine substrate is sterically unable to undergo this rearrangement, explaining H3K36me3 inactivity. Quantum mechanics/molecular mechanics (QM/MM), molecular dynamics simulations, variant analysis Inorganic chemistry Medium 38781256
2023 Cryo-EM structures of KDM2A and KDM2B trapped on nucleosome substrates (using a covalent H3K36-inhibitor conjugate) revealed that KDM2A requires the nucleosome acidic patch for nucleosome binding whereas KDM2B does not; nucleosome binding by KDM2A is facilitated by dynamic nucleosomal DNA unwrapping and histone charge shielding that mobilize the H3K36 sequence for demethylation. Cryo-electron microscopy (cryo-EM), acidic patch interactome screen, covalent substrate-inhibitor conjugate Nature chemical biology High 36797403
2011 KDM2A is specifically recruited to CpG islands via its ZF-CXXC domain through direct interaction with linker DNA at non-methylated CpG sequences; nucleosomes are a major barrier to KDM2A binding, and CpG islands are recognized through a combination of unmethylated DNA state and reduced nucleosome occlusion. Defined chromatin templates in vitro, chromatin profiling in vivo, ZF-CXXC domain biochemical characterization Molecular and cellular biology High 22083960
2014 The CxxC-ZF domain of KDM2A is required for binding to the rDNA promoter via unmethylated CpG dinucleotides in vitro and in vivo; this binding is required for KDM2A to demethylate H3K36me2 at the rDNA promoter in response to starvation and to reduce rDNA transcription. A JmjC catalytic domain mutation abolished demethylase activity and rDNA repression, while a CxxC-ZF mutation retained demethylase activity but failed to reduce rDNA transcription. Domain mutagenesis, ChIP, in vitro DNA binding, knockdown-rescue experiments Cell structure and function High 24553073
2010 KDM2A localizes to nucleoli and binds the rRNA gene (rDNA) promoter. Overexpression of KDM2A represses rRNA transcription in a demethylase-activity-dependent manner. Under starvation, KDM2A activity is stimulated, reducing H3K36me1/me2 at the rDNA promoter and suppressing rRNA transcription. Cell-permeable succinate inhibits KDM2A demethylase activity and prevents starvation-induced rRNA transcription reduction. Overexpression, knockdown, ChIP assays, nucleolar localization by microscopy, succinate inhibitor treatment The EMBO journal High 20379134
2015 Mild glucose starvation activates KDM2A through AMPK signaling to reduce H3K36me2 at the rDNA promoter and suppress rRNA transcription and cell proliferation; this pathway is distinct from TIF-IA regulation by AMPK and operates in both ER+ and triple-negative breast cancer cells. 2-DG treatment, AMPK inhibition, KDM2A knockdown, ChIP assays Molecular and cellular biology High 26416883
2019 Metformin activates KDM2A to reduce rRNA transcription and cell proliferation by a dual mechanism requiring both AMPK activation and reduction of intracellular succinate levels; AMPK activation alone is insufficient without the succinate reduction, as succinate replenishment blocks KDM2A activation but not AMPK activation. Metformin treatment, AMPK inhibition, metabolite (succinate, α-ketoglutarate) supplementation, ChIP assays, KDM2A knockdown Scientific reports Medium 31822720
2017 KDM2A integrates DNA methylation and H3K9me3 histone modification signals through a nucleosome interaction module comprising a CXXC zinc finger, a PHD domain, and a directly identified HP1-binding motif (LxVxL-type). KDM2A directly binds HP1 and can be recruited to H3K9me3-modified chromatin through HP1, while HP1 can also be recruited to unmethylated chromatin by KDM2A. A KDM2A mutant deficient in HP1-binding is inactive in an in vivo zebrafish overexpression assay. Biochemical pulldown, direct binding assays, HP1-binding motif mutagenesis, in vivo zebrafish functional assay Nucleic acids research High 28180290
2019 HP1γ directly binds KDM2A via the LxVxL motif (valine 801) of KDM2A and is required for nucleolar accumulation of KDM2A; knockdown of HP1γ or mutation of V801 reduces nucleolar KDM2A and suppresses starvation-induced reduction of rRNA transcription. Co-IP, point mutagenesis, HP1γ knockdown, nucleolar localization microscopy, ChIP Oncotarget Medium 31413816
2008 KDM2A associates with heterochromatin and directly interacts with HP1, promoting HP1 localization to chromatin. KDM2A is required to maintain the heterochromatic state (demonstrated by epigenetic reporter), associates with centromeres, and represses transcription of small non-coding RNAs encoded by centromeric satellite repeats. Forced expression of satellite RNAs compromised HP1 localization and the heterochromatic state. siRNA knockdown, epigenetic reporter system, co-IP, centromere association by immunofluorescence/ChIP, satellite RNA overexpression Cell cycle Medium 19001877
2015 ATM interacts with KDM2A; their interaction increases in response to DNA double-strand breaks. ATM specifically phosphorylates KDM2A at threonine 632 (T632) following DNA damage. T632 phosphorylation does not alter KDM2A demethylase activity but abrogates its chromatin-binding capacity, leading to increased H3K36me2 near DNA damage sites. Enriched H3K36me2 recruits the MRE11 complex via direct interaction with the BRCT2 domain of NBS1, enabling efficient DNA damage repair. Co-IP, ATM interaction assay, mutagenesis (T632 site), mass spectrometry, ChIP, DNA damage assays Oncogene High 25823024
2020 SIRT6 mono-ADP ribosylates KDM2A, leading to rapid displacement of KDM2A from chromatin, resulting in increased H3K36me2 levels at DNA damage sites; H3K36me2 then promotes H3K9 trimethylation via HP1α binding, which transiently suppresses RNA Pol II transcription initiation and recruits NHEJ factors to DSBs. SIRT6 enzymatic assay, chromatin displacement assay, H3K36me2/H3K9me3 ChIP, NHEJ factor recruitment assays Aging Medium 32584788
2013 KDM2A epigenetically represses DUSP3 expression by demethylating H3K36me2 at the DUSP3 locus in NSCLC cells. DUSP3 dephosphorylates ERK1/2, so KDM2A overexpression activates ERK1/2 signaling through epigenetic suppression of DUSP3. KDM2A knockdown/overexpression, catalytic mutant, ChIP at DUSP3 locus, ERK1/2 phosphorylation assays, rescue experiments The Journal of clinical investigation High 24200691
2014 KDM2A transcriptionally represses HDAC3 by removing H3K36me2 at the HDAC3 promoter in NSCLC cells. HDAC3 in turn represses cell cycle (CDK6) and invasion (NANOS1) genes; thus KDM2A promotes NSCLC tumorigenicity through the KDM2A→HDAC3 repression→CDK6/NANOS1 de-repression axis. KDM2A knockdown/overexpression (catalytic mutant controls), ChIP at HDAC3 promoter, HDAC3 knockdown rescue experiments, xenograft models The Journal of biological chemistry High 24482232
2017 KDM2A interacts with RelA (NF-κB subunit) and co-occupies the TET2 gene promoter to repress TET2 transcription, reducing 5'-hydroxymethylcytosine levels in genomic DNA. Depletion of RelA or KDM2A restores TET2 expression, leading to re-activation of TET2 downstream targets (EpCAM, E-cadherin) and inhibition of breast cancer invasion. Co-IP, ChIP, knockdown-rescue assays, 5-hmc level measurement, invasion assays Oncogenesis Medium 28785073
2015 Kdm2a and Kdm2b regulate the turnover of non-phosphorylated β-catenin specifically within the nucleus via direct interaction with the fourth and fifth armadillo repeats of β-catenin; the lysine residues in this region are required for methylation of non-phosphorylated β-catenin, which is demethylated by Kdm2a/b and subsequently ubiquitylated. Kdm2a/b knockdown in Xenopus embryos increases non-phosphorylated and methylated β-catenin and upregulates β-catenin target genes. Direct interaction assays (Co-IP/pulldown), β-catenin methylation-ubiquitylation assays, Xenopus embryo knockdown with phenotypic and molecular readouts Developmental cell High 26004508
2023 KDM2A promotes proteasomal degradation of TCF/LEF transcription factors (including TCF7L2) independently of its demethylase domain; this requires the KDM2A CXXC domain and is neddylation-dependent. The C-terminal region of TCF7L2 and the CXXC domain of KDM2A mediate their direct interaction. Co-IP, domain deletion/mutagenesis, proteasome inhibition, neddylation inhibition, protein stability assays Cells Medium 37998355
2020 Alternative short isoform of KDM2A (KDM2A-SF), which lacks the JmjC demethylase domain, binds to CpG island promoters via its CXXC domain and represses canonical Wnt signaling target genes (Axin2, Cyclin D1) in a demethylase-independent manner. KDM2A-SF and KDM2B-SF interact with the Wnt transcriptional mediator TCF7L1. ChIP at target promoters, luciferase reporter assays, co-IP with TCF7L1, domain deletion analysis PloS one Medium 33104714
2017 The short isoform of KDM2A (SF-KDM2A), lacking the JmjC domain, localizes to nucleoli, binds the rDNA promoter via its zf-CXXC domain, reduces H4K20me3 at the rDNA promoter, and activates rRNA transcription; CXXC domain mutation abolishes both promoter binding and rRNA transcription activation. Nucleolar localization assays, ChIP at rDNA promoter, CXXC domain mutagenesis, H4K20me3 ChIP, SF-KDM2A knockdown/overexpression International journal of oncology Medium 28350064
2023 KDM2A is required for dissolution of ALT-specific telomere clusters following recombination-directed telomere DNA synthesis; mechanistically, KDM2A promotes de-clustering of ALT multitelomeres by facilitating isopeptidase SENP6-mediated SUMO deconjugation at telomeres. Loss of KDM2A or SENP6 impairs post-recombination telomere de-SUMOylation and causes chromosome missegregation and mitotic cell death. CRISPR/Cas9 genetic screens, KDM2A/SENP6 co-epistasis, telomere SUMO assays, chromosome segregation analysis Nature communications High 36991019
2014 Fbxl11/Kdm2a knockout mice die at E10.5-12.5 with severe growth defects, decreased cell proliferation, and increased apoptosis. Loss of Fbxl11 reduces Polycomb group protein Ezh2 and PcG-mediated H2A ubiquitination, and upregulates the CDK inhibitor p21Cip1. Knockout mouse generation, histology, Western blot, immunostaining for H2A ubiquitination and p21Cip1 Mechanisms of development High 25463925
2013 KDM2A depletion in stem cells from apical papilla (SCAPs) inhibits cell proliferation and arrests the cell cycle at G1/S by de-repressing the CDK inhibitors p15INK4B and p27Kip1. ChIP assays showed that KDM2A knockdown increases H3K4 trimethylation at p15INK4B and p27Kip1 loci. shRNA knockdown, cell cycle analysis by flow cytometry, ChIP for H3K4me3 at target loci Molecular and cellular biochemistry Medium 23559091
2016 KDM2A silencing in SCAPs de-represses SFRP2 transcription by increasing H3K4 and H3K36 methylation at the SFRP2 promoter; SFRP2 enhances osteo/dentinogenic differentiation via Osterix transcription factor. BCOR functions as a co-factor of KDM2A in this regulation. KDM2A knockdown, ChIP for H3K4me/H3K36me at SFRP2 promoter, differentiation assays, BCOR knockdown Cell proliferation Medium 27074224
2013 KDM2A knockdown in SCAPs increases H3K4me3 at SOX2 and NANOG loci and upregulates these stemness genes. Co-factor BCOR knockdown similarly increases SOX2 and NANOG mRNA, suggesting BCOR acts with KDM2A to repress stemness genes. KDM2A depletion enhances adipogenic and chondrogenic differentiation. shRNA knockdown of KDM2A and BCOR, ChIP for H3K4me3, differentiation assays Experimental cell research Medium 23872478
2014 KDM2A physically binds Rb and E2F1 in a cell cycle-dependent manner and represses E2F1 transcriptional activity. ChIP assays demonstrate KDM2A associates with E2F1-regulated proliferative promoters (CDC25A, TS) in early G-phase and dissociates in S-phase. KDM2A also occupies MMP9, 14, 15, FLT1, and KDR promoters and suppresses E2F1-mediated induction of these promoters. Co-IP, ChIP at promoters, cell cycle synchronization, luciferase reporter assays PloS one Medium 25029110
2021 Myeloid-specific knockout of Kdm2a increases H3K36me2 levels at the Pparg locus with augmented chromatin accessibility and Stat6 recruitment, rendering macrophages with preferential M2 polarization. Kdm2a-deficient mice are protected from HFD-induced obesity and insulin resistance. Conditional KO (LysM-Cre), H3K36me2 ChIP at Pparg locus, ATAC-seq for chromatin accessibility, Stat6 ChIP, metabolic phenotyping Cell death and differentiation High 33462408
2024 In male germ cells, KDM2A acts as a lysine demethylase targeting H3K36me3 (in addition to H3K36me2). Conditional deletion of Kdm2a in pre-meiotic germ cells causes complete male sterility with spermatogenesis arrested at the zygotene stage. KDM2A deficiency disrupts H3K36me2/3 balance (reducing H3K36me2 and increasing H3K36me3 in c-KIT+ germ cells). KDM2A recruits transcription factor E2F1 and co-factor HCFC1 to promoters of meiosis entry/progression genes (Stra8, Meiosin, Spo11, Sycp1). Conditional KO mice (pre-meiotic specific), ChIP-seq for H3K36me2/3, Co-IP for E2F1/HCFC1, ChIP at meiotic gene promoters The EMBO journal High 39160277
2025 Conditional deletion of Kdm2a in spermatogonia using a different Cre system demonstrates Kdm2a is required for Polycomb-mediated repression during spermatogonial differentiation: KO spermatogonia show increased H3K36me2 and reduced H3K27me3 at CpG-rich gene promoters, with failed gene repression of 750+ genes. In spermatocytes, Kdm2a loss disrupts meiotic prophase, chromosome synapsis, processing of meiotic DSBs, and X-linked gene repression. Conditional KO (spermatogonia-specific Cre), RNA-seq, ChIP-seq for H3K36me2 and H3K27me3, DSB repair analysis Nature communications High 40701999
2021 KDM2A targets PFKFB3 (6-phosphofructo-2-kinase) for ubiquitylation and proteasomal degradation through its ubiquitin ligase (F-box) activity, suppressing myeloma cell proliferation and angiogenesis; this is independent of KDM2A histone demethylase activity. Co-IP, ubiquitylation assays, PFKFB3 stability/degradation assays, KDM2A overexpression/knockdown in multiple myeloma cells Frontiers in oncology Medium 34079757
2025 In skeletal muscle, Kdm2a deficiency increases H3K36me2 levels at the Esrrg locus, promoting recruitment of Mrg15 to process Esrrg precursor mRNA splicing, thereby reshaping skeletal muscle metabolic profiles to induce slow-twitch myofiber transition. Deletion or inhibition of Kdm2a shifts fuel use and protects mice against cold insults and HFD-induced obesity. Conditional KO (muscle-specific), H3K36me2 ChIP at Esrrg, Mrg15 co-IP/ChIP, mRNA splicing analysis, metabolic phenotyping Nature metabolism High 39870955
2024 KDM2A and KDM2B redundantly protect a subset of CpG islands from DNA methylation in an H3K36me2 demethylation-dependent manner; double KO of Kdm2a/2b causes stronger increase in CGI DNA methylation than single KOs. JmjC domain mutations that abolish demethylase activity phenocopy the double KO, confirming the catalytic mechanism underlies CGI protection from aberrant methylation. Kdm2a/2b single and double KO, JmjC domain catalytic mutations, DNA methylation profiling Journal of genetics and genomics High 39522683
2025 PHF8 interacts with KDM2A via two regions including an intrinsically disordered region (IDR) of KDM2A and negatively regulates KDM2A activity toward rRNA transcription; AMPK-mediated dephosphorylation of KDM2A at Ser731 (located N-terminal to the PHF8-binding region) reduces PHF8 binding and activates KDM2A. A S731A KDM2A mutant shows decreased PHF8 binding and reduced rRNA transcription. Co-IP, domain deletion mapping, S731A mutagenesis, AMPK activator treatment, rRNA transcription assays Biomolecules Medium 40427554
2025 De novo variants in KDM2A that cause intellectual disability affect KDM2A subcellular distribution, expression, and stability in human cells. Genetic epistasis in Drosophila indicated that some variants act through loss of nuclear function, while at least one variant (c.704C>T, p.Pro235Leu) also confers cytoplasmic gain-of-function toxicity, as eliminating endogenous Drosophila Kdm2 does not reproduce the neurodevelopmental phenotype. Human cell expression/localization assays for pathogenic variants, Drosophila KDM2A variant expression and Kdm2 endogenous KO epistasis, enzymatic-methylation sequencing of patient blood American journal of human genetics Medium 41468891
2023 Hepatitis B virus core protein (HBC) interacts with RANGAP1 and stabilizes it by disrupting the RANGAP1-SYVN1 (E3 ligase) interaction; stabilized RANGAP1 then interacts with KDM2A and promotes KDM2A stabilization by disrupting the KDM2A-SYVN1 interaction, thereby upregulating KDM2A to facilitate HCC cell growth and migration. Co-IP, Western blot, SYVN1-KDM2A interaction assays, stability/ubiquitination assays Cellular oncology Medium 37845585
2023 KDM2A knockdown in NSD1-deficient HNSCC reverses decreased H3K36me2 and elevated H3K27me3 at CXCL9 and CXCL10 promoters, restores T-cell chemokine expression, and enables T-cell infiltration into the tumor microenvironment. KDM2A suppression inhibited tumor growth only in immunocompetent mice, establishing KDM2A as the primary H3K36me2 demethylase whose activity is antagonistic to NSD1-dependent H3K36me2 writing. KDM2A knockdown, ChIP for H3K36me2/H3K27me3 at chemokine promoters, immunocompetent vs immunodeficient mouse tumor models Cancer research High 37311054
2025 STAT3 forms a complex specifically with NFκB p50 (not p65) that occupies the KDM2A promoter at an NFκB p50 binding motif, upregulating KDM2A expression in cancer-associated fibroblasts in response to IL-6. KDM2A-expressing CAFs secrete CXCR2-associated chemokines promoting M2 macrophage polarization. Co-IP for STAT3-NFκB p50 complex, ChIP at KDM2A promoter, pharmacological/genetic inhibition of pathway components, flow cytometry for macrophage markers Cancer cell international Medium 37821959
2024 DUX4-mediated transcription of HSATII pericentromeric satellite repeats causes nuclear foci formation of KDM2A/B-PRC1 complexes, sequestering them and causing global loss of PRC1-mediated monoubiquitination of histone H2A; this loss of PRC1-H2Aub signaling severely impairs DNA damage response. DUX4 expression, immunofluorescence for KDM2A/B-PRC1 nuclear foci, H2A ubiquitination assays, DNA damage response assays The Journal of cell biology Medium 38451221
2023 KDM2A-mediated reduction of H3K36me2 at MAPK pathway gene loci (particularly p38 MAPK pathway genes) in neural progenitor cells impairs NPC proliferation, increases apoptosis, and causes premature neuronal differentiation. De novo mutations in KDM2A identified in intellectual disability patients significantly decrease KDM2A protein levels. ChIP-seq shows KDM2A binding at transcription start sites of neurogenesis genes and H3K36me2 reduction at downstream regulatory elements upon KDM2A knockdown. KDM2A knockdown, ChIP-seq for KDM2A binding and H3K36me2, RNA-seq in neural stem cells and cerebral organoids, characterization of patient variants Neuroscience bulletin Medium 38060137
2025 RBM15-mediated m6A modification upregulates KDM2A mRNA, leading to increased KDM2A protein; elevated KDM2A reduces H3K36me2 enrichment at the HOXA2 promoter (by ChIP) to inhibit HOXA2 expression, promoting chondrocyte ferroptosis in an OA cell model. RIP assay for m6A on KDM2A mRNA, dual-luciferase assay, ChIP for H3K36me2 at HOXA2 promoter, rescue experiments Tissue & cell Medium 41349348

Source papers

Stage 0 corpus · 93 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2013 KDM2A promotes lung tumorigenesis by epigenetically enhancing ERK1/2 signaling. The Journal of clinical investigation 155 24200691
2008 KDM2A represses transcription of centromeric satellite repeats and maintains the heterochromatic state. Cell cycle (Georgetown, Tex.) 103 19001877
2010 JmjC enzyme KDM2A is a regulator of rRNA transcription in response to starvation. The EMBO journal 90 20379134
2015 Kdm2a/b Lysine Demethylases Regulate Canonical Wnt Signaling by Modulating the Stability of Nuclear β-Catenin. Developmental cell 77 26004508
2014 A molecular threading mechanism underlies Jumonji lysine demethylase KDM2A regulation of methylated H3K36. Genes & development 71 25128496
2014 The histone demethylase Fbxl11/Kdm2a plays an essential role in embryonic development by repressing cell-cycle regulators. Mechanisms of development 66 25463925
2017 Lysine demethylase KDM2A inhibits TET2 to promote DNA methylation and silencing of tumor suppressor genes in breast cancer. Oncogenesis 59 28785073
2016 Expanding the molecular signature of ossifying fibromyxoid tumors with two novel gene fusions: CREBBP-BCORL1 and KDM2A-WWTR1. Genes, chromosomes & cancer 57 27537276
2015 ATM-mediated KDM2A phosphorylation is required for the DNA damage repair. Oncogene 57 25823024
2015 Mild Glucose Starvation Induces KDM2A-Mediated H3K36me2 Demethylation through AMPK To Reduce rRNA Transcription and Cell Proliferation. Molecular and cellular biology 56 26416883
2020 Synovial Mesenchymal Stem Cell-Derived EV-Packaged miR-31 Downregulates Histone Demethylase KDM2A to Prevent Knee Osteoarthritis. Molecular therapy. Nucleic acids 55 33294294
2018 LINC00460 modulates KDM2A to promote cell proliferation and migration by targeting miR-342-3p in gastric cancer. OncoTargets and therapy 55 30323616
2014 Transcriptional repression of histone deacetylase 3 by the histone demethylase KDM2A is coupled to tumorigenicity of lung cancer cells. The Journal of biological chemistry 54 24482232
2013 Depletion of histone demethylase KDM2A enhanced the adipogenic and chondrogenic differentiation potentials of stem cells from apical papilla. Experimental cell research 54 23872478
2020 ZHX2 restricts hepatocellular carcinoma by suppressing stem cell-like traits through KDM2A-mediated H3K36 demethylation. EBioMedicine 52 32114388
2021 Kdm2a deficiency in macrophages enhances thermogenesis to protect mice against HFD-induced obesity by enhancing H3K36me2 at the Pparg locus. Cell death and differentiation 51 33462408
2014 Histone demethylase KDM2A promotes tumor cell growth and migration in gastric cancer. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 51 25245333
2016 Demethylation of SFRP2 by histone demethylase KDM2A regulated osteo-/dentinogenic differentiation of stem cells of the apical papilla. Cell proliferation 47 27074224
2016 RUNX3-mediated up-regulation of miR-29b suppresses the proliferation and migration of gastric cancer cells by targeting KDM2A. Cancer letters 47 27497248
2017 KDM2A integrates DNA and histone modification signals through a CXXC/PHD module and direct interaction with HP1. Nucleic acids research 44 28180290
2013 Depletion of histone demethylase KDM2A inhibited cell proliferation of stem cells from apical papilla by de-repression of p15INK4B and p27Kip1. Molecular and cellular biochemistry 43 23559091
2021 Histone demethylase KDM2A: Biological functions and clinical values (Review). Experimental and therapeutic medicine 38 34007332
2020 Epigallocatechin gallate reverses gastric cancer by regulating the long noncoding RNA LINC00511/miR-29b/KDM2A axis. Biochimica et biophysica acta. Molecular basis of disease 38 32512188
2020 SIRT6 mono-ADP ribosylates KDM2A to locally increase H3K36me2 at DNA damage sites to inhibit transcription and promote repair. Aging 36 32584788
2015 Integrated genomic and functional analyses of histone demethylases identify oncogenic KDM2A isoform in breast cancer. Molecular carcinogenesis 35 26207617
2022 HOXA-AS2 contributes to regulatory T cell proliferation and immune tolerance in glioma through the miR-302a/KDM2A/JAG1 axis. Cell death & disease 34 35181676
2014 Mammalian lysine histone demethylase KDM2A regulates E2F1-mediated gene transcription in breast cancer cells. PloS one 34 25029110
2011 Recognition of CpG island chromatin by KDM2A requires direct and specific interaction with linker DNA. Molecular and cellular biology 34 22083960
2018 HPV16 E7-induced upregulation of KDM2A promotes cervical cancer progression by regulating miR-132-radixin pathway. Journal of cellular physiology 31 30132864
2021 Circular RNA circFOXO3 regulates KDM2A by targeting miR-214 to promote tumor growth and metastasis in oral squamous cell carcinoma. Journal of cellular and molecular medicine 23 34117688
2023 Histone demethylase KDM2A is a selective vulnerability of cancers relying on alternative telomere maintenance. Nature communications 22 36991019
2019 Metformin activates KDM2A to reduce rRNA transcription and cell proliferation by dual regulation of AMPK activity and intracellular succinate level. Scientific reports 22 31822720
2023 Structural basis of paralog-specific KDM2A/B nucleosome recognition. Nature chemical biology 21 36797403
2021 UNC5B-AS1 promotes the proliferation, migration and EMT of hepatocellular carcinoma cells via regulating miR-4306/KDM2A axis. Cell cycle (Georgetown, Tex.) 21 34612138
2020 LncRNA LINC01278 accelerates colorectal cancer progression via miR-134-5p/KDM2A axis. European review for medical and pharmacological sciences 21 33155208
2022 Histone H3K36me2 demethylase KDM2A promotes bladder cancer progression through epigenetically silencing RARRES3. Cell death & disease 20 35697678
2018 MicroRNA‑3666 suppresses the growth and migration of glioblastoma cells by targeting KDM2A. Molecular medicine reports 20 30483744
2022 NUF2 Drives Clear Cell Renal Cell Carcinoma by Activating HMGA2 Transcription through KDM2A-mediated H3K36me2 Demethylation. International journal of biological sciences 19 35813477
2014 CxxC-ZF domain is needed for KDM2A to demethylate histone in rDNA promoter in response to starvation. Cell structure and function 18 24553073
2021 Up-regulation of miR-663a inhibits the cancer stem cell-like properties of glioma via repressing the KDM2A-mediated TGF-β/SMAD signaling pathway. Cell cycle (Georgetown, Tex.) 17 34424812
2025 Kdm2a inhibition in skeletal muscle improves metabolic flexibility in obesity. Nature metabolism 16 39870955
2020 MiR-134-5p Regulates Myocardial Apoptosis and Angiogenesis by Directly Targeting KDM2A After Myocardial Infarction. International heart journal 16 32684588
2020 Production of ROS by Gallic Acid Activates KDM2A to Reduce rRNA Transcription. Cells 16 33050392
2024 The Unique Role of the Second Coordination Sphere to Unlock and Control Catalysis in Nonheme Fe(II)/2-Oxoglutarate Histone Demethylase KDM2A. Inorganic chemistry 15 38781256
2023 Targeting KDM2A Enhances T-cell Infiltration in NSD1-Deficient Head and Neck Squamous Cell Carcinoma. Cancer research 15 37311054
2012 Lysine-specific demethylase 2A (KDM2A) normalizes human embryonic stem cell derived keratinocytes. Proceedings of the National Academy of Sciences of the United States of America 14 22635273
2022 Oocyte-Specific Knockout of Histone Lysine Demethylase KDM2a Compromises Fertility by Blocking the Development of Follicles and Oocytes. International journal of molecular sciences 13 36233308
2021 Gallic Acid Derivatives Propyl Gallate and Epigallocatechin Gallate Reduce rRNA Transcription via Induction of KDM2A Activation. Biomolecules 13 35053178
2017 SF-KDM2A binds to ribosomal RNA gene promoter, reduces H4K20me3 level, and elevates ribosomal RNA transcription in breast cancer cells. International journal of oncology 13 28350064
2021 KDM2A Targets PFKFB3 for Ubiquitylation to Inhibit the Proliferation and Angiogenesis of Multiple Myeloma Cells. Frontiers in oncology 11 34079757
2020 Alternative isoforms of KDM2A and KDM2B lysine demethylases negatively regulate canonical Wnt signaling. PloS one 11 33104714
2019 Knockdown of KDM2A inhibits proliferation associated with TGF-β expression in HEK293T cell. Molecular and cellular biochemistry 11 30604066
2025 Macrophage KDM2A promotes atherosclerosis via regulating FYN and inducing inflammatory response. International journal of biological sciences 10 40303308
2023 KDM2A interacts with estrogen receptor α to promote bisphenol A and S-induced breast cancer cell proliferation by repressing TET2 expression. Ecotoxicology and environmental safety 10 37315367
2019 Histone demethylase Kdm2a regulates germ cell genes and endogenous retroviruses in embryonic stem cells. Epigenomics 10 31172793
2017 A demethylation deficient isoform of the lysine demethylase KDM2A interacts with pericentromeric heterochromatin in an HP1a-dependent manner. Nucleus (Austin, Tex.) 10 28816576
2023 The Role of KDM2A and H3K36me2 Demethylation in Modulating MAPK Signaling During Neurodevelopment. Neuroscience bulletin 9 38060137
2019 KDM2A-dependent reduction of rRNA transcription on glucose starvation requires HP1 in cells, including triple-negative breast cancer cells. Oncotarget 9 31413816
2023 Testis-specific knockout of Kdm2a reveals nonessential roles in male fertility but partially compromises spermatogenesis. Theriogenology 8 37354760
2023 Hepatitis B virus core protein stabilizes RANGAP1 to upregulate KDM2A and facilitate hepatocarcinogenesis. Cellular oncology (Dordrecht, Netherlands) 8 37845585
2015 Spatial and temporal expression of histone demethylase, Kdm2a, during murine molar development. Biotechnic & histochemistry : official publication of the Biological Stain Commission 8 26720400
2024 DUX4-induced HSATII transcription causes KDM2A/B-PRC1 nuclear foci and impairs DNA damage response. The Journal of cell biology 7 38451221
2023 Circ_072697 knockdown promotes advanced glycation end products-induced cell proliferation and migration in HaCaT cells via miR-3150a-3p/KDM2A axis. BMC endocrine disorders 7 37726685
2023 A novel STAT3/ NFκB p50 axis regulates stromal-KDM2A to promote M2 macrophage-mediated chemoresistance in breast cancer. Cancer cell international 7 37821959
2022 KDM2A plays a dual role in regulating the expression of malignancy-related genes in esophageal squamous cell carcinoma. Biochemical and biophysical research communications 7 35932580
2021 CSNK1A1, KDM2A, and LTB4R2 Are New Druggable Vulnerabilities in Lung Cancer. Cancers 7 34298691
2021 Ablation of KDM2A Inhibits Preadipocyte Proliferation and Promotes Adipogenic Differentiation. International journal of molecular sciences 7 34575926
2024 MicroRNA-721 regulates gluconeogenesis via KDM2A-mediated epigenetic modulation in diet-induced insulin resistance in C57BL/6J mice. Biological research 6 38745315
2024 Histone demethylase KDM2A recruits HCFC1 and E2F1 to orchestrate male germ cell meiotic entry and progression. The EMBO journal 6 39160277
2023 Stabilization of nuclear β-catenin by inhibiting KDM2A mediates cerebral ischemic tolerance. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 6 36723950
2023 Maternal Kdm2a-mediated PI3K/Akt signaling and E-cadherin stimulate the morula-to-blastocyst transition revealing crucial roles in early embryonic development. Theriogenology 6 37356280
2022 Histone demethylase KDM2A suppresses EGF-TSPAN8 pathway to inhibit breast cancer cell migration and invasion in vitro. Biochemical and biophysical research communications 5 36084547
2023 Lysine Demethylase KDM2A Promotes Proteasomal Degradation of TCF/LEF Transcription Factors in a Neddylation-Dependent Manner. Cells 4 37998355
2023 Circ_0005615 promotes cervical cancer cell growth and metastasis by modulating the miR-138-5p/KDM2A axis. Journal of biochemical and molecular toxicology 3 37393518
2023 KDM2A Deficiency in the Liver Promotes Abnormal Liver Function and Potential Liver Damage. Biomolecules 3 37892137
2022 KDM2A and KDM3B as Potential Targets for the Rescue of F508del-CFTR. International journal of molecular sciences 3 36077010
2022 Knockdown of circGOLPH3 inhibits cell progression and glycolysis by targeting miR-145-5p/lysine demethylase 2A (KDM2A) axis in oral squamous cell carcinoma. Head & neck 3 36268878
2025 Inhibition of SCFKDM2A/USP22-dependent nuclear β-catenin ubiquitylation mediates cerebral ischemic tolerance. Communications biology 2 39934243
2025 Conditional Knockout Kdm2a Reveals Crucial Involvement in Development and Function of Kidney Collecting Ducts. International journal of molecular sciences 2 39940999
2025 De novo variants in KDM2A cause a syndromic neurodevelopmental disorder. medRxiv : the preprint server for health sciences 2 40236430
2015 [A CxxC domain that binds to unmethylated CpG is required for KDM2A to control rDNA transcription]. Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan 2 25743893
2025 Interaction Between PHF8 and a Segment of KDM2A, Which Is Controlled by the Phosphorylation Status at a Specific Serine in an Intrinsically Disordered Region of KDM2A, Regulates rRNA Transcription and Cell Proliferation in a Breast Cancer Cell Line. Biomolecules 1 40427554
2025 Sodium butyrate promotes enteric glial cells neurogenesis by inhibiting Kdm2a and inducing Klf4 expression. Journal of pediatric surgery 1 40571091
2025 RBM15-mediated m6A modification upregulates KDM2A to promote ferroptosis in osteoarthritis cells. Tissue & cell 1 41349348
2025 KDM2A demethylase: A versatile epigenetic regulator in development, cancer, and therapeutic horizons. Pathology, research and practice 1 41411802
2025 De novo variants in KDM2A cause a syndromic neurodevelopmental disorder. American journal of human genetics 1 41468891
2024 KDM2A and KDM2B protect a subset of CpG islands from DNA methylation. Journal of genetics and genomics = Yi chuan xue bao 1 39522683
2026 Tumor Cell Clustering Enhances Metastatic Competence by Regulating the H3K36 Histone Demethylase KDM2A. bioRxiv : the preprint server for biology 0 41648535
2026 Inhibition of Kdm2a with Daminozide suppresses high myopia progression and related neuropsychiatric comorbidities by epigenetically modulating the gut-eye axis. Pharmacological research 0 41698562
2025 The histone H3 lysine 36 demethylase KDM2A/FBXL11 controls Polycomb-mediated gene repression and germ cell development in male mice. Nature communications 0 40701999
2025 Vitamin C rescues embryonic developmental arrest caused by maternal Kdm2a deficiency via regulating PTEN/PI3K/AKT axis. Theriogenology 0 41192032
2025 SLC25A11 Is Associated with KDM2A-Dependent Reduction in rRNA Transcription Induced by Aminooxyacetic Acid. Cells 0 41227300
2023 Histone demethylase KDM2A is a selective vulnerability of cancers relying on alternative telomere maintenance. bioRxiv : the preprint server for biology 0 36798426

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