| 2012 |
KDM3B possesses histone H3K9-me1/2 demethylase activity (via its JmjC domain) and activates leukemogenic oncogene LMO2 expression through a synergistic interaction with the histone acetyltransferase CBP, forming a co-activator complex at the LMO2 locus. |
ChIP-chip genome-wide occupancy analysis, in vitro demethylase activity assays, co-immunoprecipitation, transcriptional reporter assays in HL-60 cells |
Molecular and cellular biology |
High |
22615488
|
| 2015 |
Kdm3b demethylates H3K9me1/2 in vivo; knockout mice show elevated H3K9me1/2/3 in ovary and uterus, reduced circulating IGF-1 (via decreased renal IGFBP-3 expression), reduced 17β-estradiol, and defects in postnatal growth, ovulation, fertilization, and uterine decidual response. |
Kdm3b knockout mouse model, hormone measurements (RIA/ELISA), histology, ChIP, gene expression analysis |
International journal of biological sciences |
High |
25892958
|
| 2015 |
KDM3B represses ANGPT1 transcription independently of its JmjC-domain H3K9 demethylase catalytic activity, instead acting through physical interaction with the co-repressor SMRT at the ANGPT1 promoter. |
Co-immunoprecipitation, ChIP at ANGPT1 promoter, JmjC-domain mutant analysis, MTT and wound-healing assays |
BMB reports |
Medium |
25413303
|
| 2015 |
Kdm3b knockout male mice show reduced spermatogenesis (44% fewer mature sperm), decreased sperm motility, and markedly reduced circulating 17β-estradiol, without changes in testosterone or androgen receptor target genes, indicating Kdm3b-mediated H3K9 demethylation is required for spermatogenesis and male sexual behavior. |
Kdm3b knockout mouse model, sperm counts, motility assays, hormone measurements, gene expression analysis |
International journal of biological sciences |
High |
26681924
|
| 2017 |
KDM3B binds retinoic acid response elements (RARE) in the HOXA1 locus (not the promoter directly) and regulates HOXA1 expression by modulating H3K9 monomethylation and dimethylation specifically at RARE; KDM3B knockdown increases H3K9me1 but decreases H3K9me2 at RARE. |
ChIP at RARE and HOXA1 promoter, KDM3B knockdown, real-time PCR, Western blot, microarray profiling |
Leukemia & lymphoma |
Medium |
28540746
|
| 2018 |
KDM3B knockout in HepG2 hepatocarcinoma cells retards cell cycle and proliferation, induces mitotic spindle multipolarity (~30% of cells), and downregulates cell-cycle genes including CDC123; additionally, Cyclin D1 protein is reduced post-translationally via proteasomal degradation without changes in CCND1 mRNA. |
CRISPR/Cas9 knockout, RNA-seq, flow cytometry, immunofluorescence for spindle multipolarity, Western blot, proteasome inhibitor assay |
Biochemical and biophysical research communications |
Medium |
30514438
|
| 2019 |
KDM3B knockdown in NB4 APL cells alters global distribution of H3K9me1/2, increases chromatin accessibility (ATAC-seq), promotes cell-cycle progression, and inhibits ATRA-induced degradation of the PML/RARα oncoprotein, indicating KDM3B maintains chromatin compaction to facilitate PML/RARα degradation. |
KDM3B knockdown, ChIP-seq, ATAC-seq, flow cytometry, Western blot for PML/RARα |
Cancer cell international |
High |
31592194
|
| 2019 |
KDM3B enzymatic activity (H3K9 demethylase) is required for its role in supporting CRPC cell proliferation; genetic rescue of KDM3B knockout with catalytically inactive KDM3B failed to restore proliferation. KDM3B loss in CRPC cells downregulates metabolic enzymes ARG2 and RDH11 and causes decreases in critical amino acids. |
shRNA screen, CRISPR/Cas9 knockout, enzymatically-inactive KDM3B rescue experiment, transcriptome analysis, metabolomics |
Oncogene |
High |
31822799
|
| 2020 |
KDM3B overexpression protects against ferroptosis induced by Erastin (an SLC7A11 inhibitor) by upregulating SLC7A11 expression through cooperation with the transcription factor ATF4, and KDM3B overexpression decreases global H3K9 methylation in HT-1080 cells. |
KDM3B overexpression in HT-1080 cells, cell viability assays, Western blot, co-immunoprecipitation with ATF4, RT-PCR |
FEBS open bio |
Medium |
32107878
|
| 2020 |
JMJD1B (KDM3B) depletion increases protein levels of the histone chaperone tNASP, causing accumulation of newly synthesized histones H3 and H4 at early steps of the histone maturation cascade and perturbing chromatin assembly, establishing a role for KDM3B in histone supply and genome stability. |
JMJD1B knockdown, Western blot for tNASP and histones, chromatin assembly assay, fractionation |
Epigenetics & chromatin |
Medium |
32070414
|
| 2020 |
KDM3B level increases in nutrient-deprived HCT116 cells and activates autophagy-related genes by demethylating H3K9me2 at their promoters; KDM3B depletion inhibits autophagic flux. |
KDM3B knockdown/overexpression, ChIP at autophagy gene promoters, H3K9me2 measurement, autophagic flux assay (LC3 puncta, Western blot) |
PloS one |
Medium |
32716961
|
| 2021 |
KDM3A and KDM3B form a protein complex (demonstrated by IP-MS) that cooperates with core pluripotency transcription factors OCT4 and SOX2 to maintain H3K9me2/3 hypomethylation at pluripotency genes; co-depletion of KDM3A and KDM3B collapses the pluripotency gene regulatory network in porcine iPSCs. |
Immunoprecipitation–mass spectrometry (IP-MS), ChIP-seq, KDM3A/KDM3B co-depletion, genome-wide regulation analysis |
FASEB journal |
Medium |
34042215
|
| 2021 |
Heterozygous Kdm3b knockout mice show increased H3K9 dimethylation selectively in the granule cell layer of the cerebellum, impaired consolidation of cerebellum-dependent motor memory (optokinetic response learning), and altered expression of plasticity-related genes in the cerebellum. |
Heterozygous Kdm3b knockout mouse, optokinetic response behavioral assay, ChIP for H3K9me2, RNA-seq |
Molecular brain |
Medium |
34217333
|
| 2022 |
KDM3B downregulation (via siRNA) increases stability of F508del-CFTR protein and boosts functional rescue of the CFTR channel, suggesting KDM3B-mediated demethylation of CFTR lysine residues promotes CFTR ubiquitination and proteasomal degradation. |
siRNA library screen against human demethylases, CFTR stability assay, channel function assay (halide-sensitive YFP), Western blot |
International journal of molecular sciences |
Low |
36077010
|
| 2024 |
KDM3B selectively binds and is inhibited by small molecules P3FI-63 and P3FI-90; biophysical binding of P3FI-90 to KDM3B demonstrated by NMR and surface plasmon resonance (SPR); enzymatic assays confirm inhibition of KDM3B (highest selectivity among KDMs tested); combined knockdown of KDM3B and KDM1A phenocopies the inhibitor effects on PAX3-FOXO1 transcriptional activity and FP-RMS growth in vitro and in vivo. |
Enzymatic KDM inhibition assays, NMR, SPR biophysical binding, RNA-seq, ATAC-seq, genetic knockdown, in vitro and in vivo tumor models |
Nature communications |
High |
38402212
|
| 2024 |
Loss of Kdm3b in IDH2- and TET2-mutant hematopoietic stem and progenitor cells (HSPCs) specifically reduces their fitness; Kdm3b loss leads to decreased expression of cytokine receptors including Mpl, rendering mutant HSPCs preferentially susceptible to JAK2 signaling inhibition. |
CRISPR/Cas9 screens in primary HSPCs ex vivo co-culture, gene expression analysis, genetic validation, JAK2 inhibitor treatment |
Cancer discovery |
Medium |
38819218
|
| 2024 |
Kdm3b loss in mouse retinal cone photoreceptors leads to accumulation of H3K9me1/2 at synapse assembly and vesicle transport genes (silencing them) and loss of H3K9me heterochromatin at apoptotic genes (activating them), resulting in cone photoreceptor apoptosis and altered cone ribbon synapse morphology. |
Kdm3b conditional knockout (retina), single-cell RNA-seq, ChIP-seq/CUT&TAG, ATAC-seq, immunofluorescence, histology |
iScience |
High |
39165843
|
| 2025 |
KDM3B regulates postradiation fibrosis in prostate stroma by maintaining N6-methyladenosine (m6A) modification on LOX mRNA; reduced KDM3B expression (driven by rs17599026 SNP via circRNA/miRNA mechanisms) decreases m6A modification of LOX mRNA, increasing its stability and LOX protein expression, which promotes collagen cross-linking and fibrosis. α-ketoglutarate supplementation restores KDM3B protein levels, reduces LOX, and mitigates fibrosis. |
CRISPR-dead Cas9 prime editing to mimic SNP, RNA immunoprecipitation, transcript stability assay, Western blot, murine fibrosis model, α-KG supplementation |
International journal of radiation oncology, biology, physics |
Medium |
40588066
|
| 2025 |
KDM3B promotes neural invasion in colorectal cancer by demethylating H3K9me2 at the NTRK1 (TrkA) locus, increasing TrkA expression, which enables nerve growth factor (NGF) binding and downstream signaling to drive neural invasion. |
CUT&TAG, ATAC-seq, shKDM3B CRC cell line, in vivo and in vitro neural invasion assays, Western blot, clinical tissue TMT-proteomics |
iScience |
Medium |
41488357
|
| 2025 |
KDM3A and KDM3B interact with RNA processing factors EFTUD2 and PRMT5 (by proteomic analysis); acute degradation of KDM3A/KDM3B causes altered alternative splicing in mESCs independent of H3K9me2 status or catalytic activity, affecting splicing of chromatin/transcription factor genes including Dnmt3b and Tcf12. |
Proteomic analysis (co-IP/MS), auxin-inducible degron acute protein degradation, RNA-seq for splicing changes, H3K9me2 ChIP-seq, catalytic mutant comparison |
iScience |
Medium |
40510131
|
| 2025 |
JMJD1B (KDM3B) acts as an arginine demethylase for FEN1 R192; JMJD1B-mediated demethylation of FEN1 R192 promotes FEN1 dissociation from PCNA and LIG1 recruitment during Okazaki fragment maturation; loss of JMJD1B causes unprocessed 5' flaps, induction of PARP1-dependent LIG3 recruitment, and DNA mutations (duplications). |
In vitro demethylation assay, PCNA binding assays, Jmjd1b knockout cells, FEN1 R192Q mutant analysis, DNA replication and mutagenesis assays |
bioRxivpreprint |
Medium |
41280084
|
| 2026 |
KDM3B targets the SHP1 gene promoter by reducing H3K9me2 levels, thereby upregulating SHP1 expression; SHP1 suppresses STING signaling, so KDM3B inhibition attenuates SHP1-mediated STING inactivation, triggering type I interferon responses and CD8+ T cell recruitment in TNBC models. |
KDM3B knockout, ChIP for H3K9me2 at SHP1 promoter, Western blot, STING pathway analysis, in vivo tumor models with immune cell profiling, KDM3B inhibitor (P3FI-90) treatment |
Advanced science |
Medium |
42201640
|