| 2012 |
KDM6B (JMJD3) promotes osteogenic differentiation of human MSCs by removing repressive H3K27me3 marks at HOX gene loci, thereby activating HOX expression and driving osteogenic commitment at the expense of adipogenic differentiation. |
shRNA knockdown, ChIP assays, overexpression in human MSCs with osteogenic/adipogenic differentiation readouts |
Cell Stem Cell |
High |
22770241
|
| 2012 |
KDM6B promotes TGF-β-induced epithelial-mesenchymal transition (EMT) in mammary epithelial cells by removing H3K27me3 marks at the SNAI1 promoter, thereby stimulating SNAI1 expression and downstream mesenchymal gene induction. |
shRNA knockdown, overexpression, ChIP assays, TGF-β-induced EMT assays in mammary epithelial cells |
The Journal of Biological Chemistry |
High |
23152497
|
| 2013 |
JMJD3 (KDM6B) inhibits somatic cell reprogramming to iPSCs through two pathways: (1) H3K27me3 demethylase-dependent upregulation of INK4a/Arf, and (2) a demethylase-independent pathway in which JMJD3 recruits the E3 ubiquitin ligase TRIM26 to target PHF20 for ubiquitination and degradation. |
Genetic KO/OE in MEFs, iPSC colony assays, Co-IP for JMJD3-TRIM26 interaction, ubiquitination assays, active-site mutant analysis |
Cell |
High |
23452852
|
| 2011 |
KDM6B expression is induced by vitamin D receptor (VDR) signaling in a VDR-dependent, cycloheximide-sensitive manner; KDM6B then co-mediates 1,25(OH)2D3-induced target gene expression and an epithelial adhesive phenotype in colon cancer cells by modulating H3K27me3 at target gene promoters. |
shRNA knockdown, inactive mutant expression, promoter activation assays, ChIP, cycloheximide treatment in SW480-ADH colon cancer cells |
Human Molecular Genetics |
High |
21890490
|
| 2012 |
JMJD3 facilitates RNA polymerase II progression through H3K27me3-enriched gene bodies of TGF-β-responsive genes by demethylating H3K27me3 along intragenic regions, enabling transcriptional elongation. |
ChIP-seq, ChIP-qPCR, genome-wide analysis of RNAPII and JMJD3 co-localization upon TGF-β treatment |
Molecular Biology of the Cell |
High |
23243002
|
| 2013 |
Jmjd3 reduces H3K27me3 marks at the Brachyury promoter and facilitates recruitment of β-catenin, enabling Wnt-signal-induced mesoderm differentiation; Jmjd3 ablation in mouse ESCs compromises mesoderm and subsequent endothelial and cardiac differentiation without affecting pluripotency. |
Jmjd3 ablation in mouse ESCs, ChIP assays at Brachyury promoter, differentiation assays |
Circulation Research |
High |
23856522
|
| 2013 |
KDM6B and EED (PRC2 component) combinatorially regulate the first mammalian cell lineage commitment: relative KDM6B/EED levels determine H3K27me3 deposition at CDX2 and GATA3 chromatin domains, activating these TE-specific master regulators in trophectoderm and repressing them in ICM; KDM6B depletion combined with EED gain-of-function abrogates CDX2/GATA3 expression and prevents embryo implantation. |
Gain- and loss-of-function in preimplantation mouse embryos, ChIP, PRC2 recruitment assays |
Molecular and Cellular Biology |
High |
23671187
|
| 2014 |
JMJD3 interacts with tumor suppressor p53 via the p53 tetramerization domain; following DNA damage, JMJD3 is transcriptionally upregulated and is recruited in a p53-dependent manner to p53 target promoters and enhancers genome-wide, where it removes H3K27me3/me2 to permit H3K27 acetylation. |
Co-IP, genome-wide ChIP-seq of JMJD3, DNA damage assays, p53-dependent recruitment experiments |
PLoS One |
High |
24797517
|
| 2014 |
Histone demethylase Jmjd3 is required for differentiation of PKC-positive rod-ON bipolar cells in the retina by enabling lineage-specific H3K27me3 demethylation at the Bhlhb4 locus; overexpression of Bhlhb4 rescues the loss of these cells in Jmjd3-knockdown retina. |
Jmjd3 loss-of-function in developing retina, ChIP at Bhlhb4 locus, Bhlhb4 rescue overexpression |
PNAS |
High |
24572572
|
| 2015 |
Jmjd3 and Utx redundantly promote H3K27me3 removal at a subset of genes required for terminal thymocyte differentiation, most critically at the S1pr1 locus (encoding a sphingosine-1-phosphate receptor for thymocyte egress); the catalytic demethylase activity is required, as the catalytically inactive Uty homolog cannot rescue S1pr1 expression. |
Conditional inactivation of Jmjd3 and Utx in intrathymic CD4+ T-cell precursors in mice, ChIP for H3K27me3, RNA analysis, rescue experiments with catalytically inactive Uty |
Nature Communications |
High |
26328764
|
| 2015 |
Jmjd3-catalyzed removal of H3K27me3, in part through recruitment by the transcription factor Rreb1, is required for expression of BAT-selective genes and development of brown adipocytes; a significant subset of BAT-selective (but not common fat or WAT-selective) genes are demarcated by H3K27me3 in preadipocytes. |
Jmjd3 gain- and loss-of-function transgenic mice, ChIP-seq for H3K27me3, adipocyte differentiation assays in vitro and in vivo, Rreb1-mediated recruitment assays |
Developmental Cell |
High |
26625958
|
| 2016 |
JMJD3 interacts with NF-κB in keratinocytes and cooperates to demethylate H3K27me3 at promoters of inflammatory, matrix metalloproteinase, and growth factor genes, driving keratinocyte wound healing; inactivation of either JMJD3 or NF-κB impairs wound healing. |
Co-IP for JMJD3-NF-κB interaction, ChIP at gene promoters, JMJD3/NF-κB knockdown in vitro and in vivo wound healing models |
Journal of Investigative Dermatology |
High |
26802933
|
| 2016 |
JMJD3 and NF-κB cooperate to activate Notch1 expression by demethylating H3K27me3 at the Notch1 promoter in wounded keratinocytes; Notch1 then activates RhoU and PLAU to promote filopodia formation and cell migration during wound healing. |
ChIP assays at Notch1 promoter, knockdown/inactivation of JMJD3, NF-κB, and Notch1 in vitro and in vivo wound models |
Scientific Reports |
High |
28747631
|
| 2016 |
JMJD3 physically interacts with ISL1 in cardiac progenitor cells; ISL1 recruits JMJD3 to enhancers of cardiac transcription factor genes (Myocd, Mef2c) and modulates its H3K27me3 demethylase activity; conditional depletion of JMJD3 impairs cardiac progenitor differentiation, phenocopying ISL1 depletion. |
Co-IP of ISL1-JMJD3, ChIP at Myocd and Mef2c enhancers, conditional JMJD3 deletion in cardiac progenitors, ESC differentiation assays |
Nucleic Acids Research |
High |
27105846
|
| 2016 |
Neuronal stimulation (NMDA) induces CREB-p/CBP-dependent and JMJD3-dependent H3K27me3 demethylation at Bdnf promoters II and VI in mature hippocampal neurons, displacing EZH2 and enabling fast Bdnf transcription; JMJD3-mediated demethylation facilitates RNAPII progression through Polycomb-repressed Bdnf loci. |
ChIP in hippocampal neurons, NMDA stimulation, EZH2 displacement assays, histone mark analysis |
Nature Communications |
Medium |
27010597
|
| 2017 |
DHEA activates TrkA phosphorylation, which triggers an Akt1/2-CREB signaling cascade that induces Jmjd3 expression in microglia; Jmjd3 then controls inflammatory gene expression and microglial polarization, mediating DHEA's anti-inflammatory effects. |
In vivo LPS-induced neuroinflammation mouse model, in vitro microglia culture, pathway inhibitor studies, Jmjd3 KD |
Molecular Psychiatry |
Medium |
28894299
|
| 2017 |
STAT3 binds the Jmjd3 promoter and represses its transcription in glioblastoma stem cells; STAT3 inhibition leads to Jmjd3 upregulation and H3K27 demethylation of neural differentiation genes; Jmjd3 overexpression slows glioblastoma stem cell growth and neurosphere formation. |
ChIP of STAT3 at Jmjd3 promoter, STAT3 inhibitor treatment, Jmjd3 KD and OE, neurosphere formation assays |
PLoS One |
Medium |
28384648
|
| 2017 |
KDM6B is required for activity-regulated neuronal survival preconditioning; Kdm6b knockdown abolishes bicuculline/4-AP-induced preconditioning of neuronal survival and impairs inducibility of a discrete set of inflammation-related genes without broadly disrupting activity-regulated transcription. |
Kdm6b KD in cultured hippocampal neurons, bicuculline/4-AP stimulation, RNA-seq, cell survival assays, pilocarpine-induced seizure in vivo |
Molecular and Cellular Neurosciences |
Medium |
24983519
|
| 2018 |
JMJD3, together with SIRT1 and PPARα, forms a positive autoregulatory loop activated by fasting-induced PKA signaling; JMJD3 acts as a gene-specific transcriptional partner of SIRT1 and epigenetically activates mitochondrial β-oxidation genes (Fgf21, Cpt1a, Mcad) by removing H3K27me3, without affecting gluconeogenic genes; liver-specific Jmjd3 knockdown causes intrinsic β-oxidation defects, hepatosteatosis, and glucose/insulin intolerance. |
Liver-specific KD, Co-IP of JMJD3-SIRT1-PPARα complex, ChIP at β-oxidation gene promoters, in vivo metabolic phenotyping in diet-induced obese mice |
Journal of Clinical Investigation |
High |
29911994
|
| 2018 |
JMJD3 is recruited to the β-MHC promoter in cardiomyocytes where it demethylates H3K27me3, promoting β-MHC expression and cardiac hypertrophy; overexpression of wild-type but not demethylase-defective JMJD3 induces hypertrophy, and JMJD3 silencing or GSK-J4 suppresses ISO-induced hypertrophy. |
ChIP at β-MHC promoter, WT vs. catalytic mutant JMJD3 overexpression, JMJD3 siRNA, GSK-J4 inhibitor treatment, in vivo isoproterenol model |
Molecular and Cellular Endocrinology |
High |
29753027
|
| 2019 |
JMJD3 forms a novel complex with the RNA helicase DDX21; this JMJD3-DDX21 complex is recruited to the ENPP2 locus (via a distant enhancer) in a JMJD3-dependent and NF-κB-dependent manner upon LPS stimulation, where DDX21 resolves R-loops formed by nascent transcripts to promote ENPP2 transcription; JMJD3's role at ENPP2 is non-enzymatic (demethylase-independent). |
Mass spectrometry identification of JMJD3 interactors, Co-IP of JMJD3-DDX21, ChIP at ENPP2 locus, CRISPR-Cas9 enhancer deletion, R-loop detection assays |
Nucleic Acids Research |
High |
31251802
|
| 2019 |
JMJD3 binds the promoter and gene body of the Pdlim4 gene by interacting with the zinc-finger transcription factor KLF2; JMJD3 deficiency in CD4+ T cells reduces PDLIM4 expression, impairing PDLIM4-mediated interaction between S1P1 and F-actin and thereby disrupting T cell trafficking from thymus to secondary lymphoid organs. |
Gene profiling and ChIP-seq in JMJD3-KO CD4+ T cells, Co-IP for JMJD3-KLF2, PDLIM4-S1P1-F-actin interaction assays, T cell trafficking experiments |
Journal of Clinical Investigation |
High |
31393857
|
| 2019 |
Kdm6b is required for hematopoietic stem cell (HSC) self-renewal under inflammatory/proliferative stress; loss of Kdm6b leads to increased AP-1 transcription factor complex (Fos/Jun) and IER gene expression independently of H3K27me3 chromatin changes; targeting AP-1 restores function of Kdm6b-deficient HSCs, demonstrating a demethylase-independent mechanism. |
Conditional Kdm6b KO mice, HSC functional assays (repopulation), RNA-seq, AP-1 genetic targeting as epistasis rescue |
Leukemia |
High |
30936419
|
| 2020 |
Temperature-dependent sex determination in turtle embryos is mediated by STAT3 phosphorylation at the female-producing (warmer) temperature; pSTAT3 binds the Kdm6b locus and represses Kdm6b transcription; Ca2+ influx (elevated at female temperature) mediates STAT3 phosphorylation, creating a temperature-sensitive regulatory cascade that blocks the male developmental pathway. |
STAT3 phosphorylation assays at different temperatures, ChIP of pSTAT3 at Kdm6b locus, Ca2+ influx measurements, Kdm6b transcription assays |
Science |
High |
32299951
|
| 2020 |
JMJD3 in macrophages is regulated by KDM6B expression downstream of JAK/STAT and NF-κB pathways; palmitate (via TLR4/MyD88 signaling) induces Jmjd3 expression, causing removal of H3K27me3 from NF-κB-mediated inflammatory gene promoters and driving macrophage inflammatory activation in diabetic peripheral tissue. |
Tlr4-/- and MyD88-/- mice, palmitate treatment, ChIP at inflammatory gene promoters, GSK-J4 inhibitor in diabetic wound healing model |
European Journal of Immunology |
High |
32662520
|
| 2021 |
Interferon-β controls the cellular α-ketoglutarate/succinate ratio (by increasing itaconate and succinate while restricting α-ketoglutarate); this metabolic shift potently blocks the JMJD3-IRF4-dependent pathway in macrophages, suppressing M2 polarization; supplementing α-ketoglutarate reverses IFNβ-mediated suppression of JMJD3-IRF4 responses. |
Metabolic flux analysis (glutamine carbon tracing), JMJD3-IRF4 pathway assays in GM-CSF/IL-4-activated macrophages, α-ketoglutarate supplementation rescue |
Cell Reports |
High |
35443173
|
| 2021 |
JMJD3 in macrophages drives NF-κB-mediated inflammatory gene transcription via H3K27me3 removal; interferon-β regulates Jmjd3 expression via JAK/STAT; myeloid-specific JMJD3 genetic depletion (Jmjd3f/f Lyz2Cre+) preserves repressive H3K27me3 on inflammatory gene promoters and reduces AAA expansion in vivo. |
Single-cell RNA-seq of human AAA tissue, myeloid-specific KO mice, elastase/angiotensin II AAA models, ChIP for H3K27me3 at inflammatory gene promoters, pharmacological inhibition |
Journal of Experimental Medicine |
High |
33779682
|
| 2021 |
JMJD3 promotes muscle stem cell (MuSC) adaptation to inflammation by removing H3K27me3 marks at the Has2 locus, initiating hyaluronic acid production via HAS2; this extracellular hyaluronic acid establishes a matrix that integrates signals directing MuSCs to exit quiescence; UTX does not substitute for JMJD3 in this process. |
Conditional KO of Jmjd3 vs. Utx in MuSCs, ChIP at Has2 locus, hyaluronic acid quantification, MuSC cell cycle re-entry assays |
Science |
High |
35926054
|
| 2021 |
KDM6B promotes CDK4/6-pRB-E2F oncogenic pathway activity in MYCN-amplified neuroblastoma by maintaining H3K4me1 enhancer marks and chromatin accessibility at CTCF/BORIS binding sites; KDM6B inhibition increases H3K27me3 but decreases H3K4me1 at these sites, disrupting long-range chromatin interactions of MYCN and E2F target genes. |
KDM6B inhibition (GSK-J4), ChIP for H3K27me3 and H3K4me1, ATAC-seq for chromatin accessibility, CDK4/6 overexpression and Rb1 KO as resistance experiments |
Nature Communications |
High |
34893606
|
| 2021 |
KDM6B promotes lung metastasis of osteosarcoma by directly mediating H3K27me3 demethylation at the LDHA gene locus, increasing LDHA expression and aerobic glycolysis; LDHA overexpression rescues the anti-metastatic phenotype of KDM6B knockdown. |
ChIP-seq and RNA-seq combined, ChIP-qPCR at LDHA locus, glycolysis assays, in vivo orthotopic lung metastasis model, LDHA rescue overexpression |
Theranostics |
High |
33664867
|
| 2021 |
KDM6B is an androgen receptor (AR)-regulated gene; AR decreases KDM6B transcription; KDM6B demethylates H3K27me3 at the cyclin D1 promoter and cooperates with Smad2/3 to promote cyclin D1 expression and prostate cancer cell proliferation. |
ChIP at cyclin D1 promoter, AR regulation of KDM6B promoter, Co-immunoprecipitation of KDM6B-Smad2/3, in vitro and in vivo PCa models |
Cell Death & Disease |
Medium |
33414463
|
| 2021 |
miR-15b targets and inhibits USP7; USP7 deubiquitinates and stabilizes KDM6B protein (MG132 increases KDM6B expression); reduced KDM6B (via miR-15b/USP7 axis) impairs osteoblast autophagy and differentiation in osteoporosis. |
miR-15b/USP7 binding validation, MG132 proteasome inhibitor experiments, USP7 OE restoring KDM6B, KDM6B KD in osteoblasts, in vivo OVX model |
Journal of Cellular and Molecular Medicine |
Medium |
33434305
|
| 2021 |
KDM6B is required for virus-specific CD8+ T cell differentiation; rapid KDM6B upregulation prior to the first cell division initiates H3K27me3 removal at genes essential for T cell proliferation and differentiation; KDM6B inhibition limits the magnitude of primary CD8+ T cell responses and memory formation. |
Genome-wide ChIP-seq for H3K27me3, ATAC-seq, RNA-seq at early time points after naive CD8+ T cell activation, KDM6B inhibition (GSK-J4), in vivo viral challenge |
Cell Reports |
High |
33730567
|
| 2021 |
The lncRNA DNM3OS physically interacts with KDM6B in the nucleus; this association induces TIAM1 expression through reduction of H3K27me3 at the TIAM1 promoter, promoting hepatocellular carcinoma proliferation, invasion, and metastasis driven by tumor-associated MSC-conditioned medium. |
Co-IP of DNM3OS-KDM6B, ChIP at TIAM1 promoter, KD/OE experiments, in vitro and in vivo HCC models |
Cancer Letters |
Medium |
33472090
|
| 2018 |
KDM6B expression is upregulated by hypoxia (1% O2 or chemical mimics) in a HIF-2α-dependent manner (not HIF-1α); HIF-2α binds a hypoxia response element in the KDM6B promoter; KDM6B forms a complex with both HIF-2α and HIF-1α and acts as a potential co-activator of HIF-α target genes. |
RNAi for HIF-1α and HIF-2α, ChIP at KDM6B promoter (HRE), Co-IP of KDM6B-HIF-2α/HIF-1α, KDM6B KD effect on HIF-2α targets |
Acta Biochimica et Biophysica Sinica |
Medium |
25520177
|
| 2021 |
KDM6B inhibition in myeloid cells (via genetic Kdm6b deletion or pharmacological GSK-J4 treatment) enhances antigen presentation, interferon response, and phagocytosis in myeloid cells by inhibiting mediators of immune suppression including Mafb, Socs3, and Sirpa; myeloid-specific Kdm6b deletion improves survival in glioblastoma mouse models and synergizes with anti-PD1 therapy. |
Single-cell and spatial transcriptomics, myeloid-specific Kdm6b KO mice (with GBM model), mechanistic studies of Mafb/Socs3/Sirpa, anti-PD1 combination experiments |
Nature Cancer |
High |
37653141
|
| 2022 |
KDM6B cooperates with Tau protein in neurons; Tau interacts with and recruits KDM6B to the promoters of Slc17a7 (VGLUT1) and Slc17a6 (VGLUT2) genes, reducing H3K27me3 levels and inducing VGLUT1/2 expression; conditional KDM6B KO in excitatory neurons reduces spine density, synaptic vesicle number, and impairs learning and memory. |
KDM6B conditional KO in excitatory neurons, Co-IP of KDM6B-Tau, ChIP at VGLUT1/2 promoters, electrophysiology, behavioral tests |
Molecular Psychiatry |
High |
36028572
|
| 2022 |
JMJD3 in wound macrophages directs early inflammation via JAK1,3/STAT3 signaling; in diabetic wounds, late IL-6-mediated JAK/STAT3 signaling sustains JMJD3 expression, which induces NF-κB-mediated inflammatory transcription via H3K27me3 removal; JMJD3-deficient myeloid cells show elevated STING (Tmem173) gene expression. |
scRNA-seq of human diabetic wounds, Jmjd3f/f Lyz2Cre+ mice, JAK/STAT pathway inhibitors, RNA-seq of wound macrophages, nanoparticle-based JMJD3 inhibition in vivo |
Cellular & Molecular Immunology |
High |
36127466
|
| 2022 |
JMJD3 promotes cardiac fibrosis by demethylating H3K27me3 at the β-catenin promoter in activated cardiac fibroblasts, increasing β-catenin expression and downstream fibrogenic gene transcription (fibronectin, CTGF, collagen I/III); JMJD3 expression is induced by angiotensin II. |
ChIP at β-catenin promoter, JMJD3 inhibition (GSK-J4), β-catenin genetic KO, in vivo myocardial infarction model with JMJD3 inhibition |
Biochemical and Biophysical Research Communications |
Medium |
32513540
|
| 2022 |
Kdm6b regulates motor neuron subtype diversification in the mouse spinal cord by acquiring cell fate specificity together with the transcription factor complex Isl1-Lhx3; Kdm6b promotes medial (MMC) and hypaxial (HMC) motor column fates while inhibiting lateral (LMC) and preganglionic (PGC) identities. |
Conditional Kdm6b KO in mouse motor neurons, single-cell RNA-seq, Isl1-Lhx3 transcription factor complex studies |
Nature Communications |
High |
35177643
|
| 2021 |
KDM6B regulates HIF-1α-mediated transcriptional activation of Nox4 under intermittent hypoxia (IH) in an HIF-1-independent manner; pharmacological KDM6B blockade or shRNA silencing abolishes IH-induced HIF-1α binding to the Nox4 HRE promoter and prevents elevated catecholamines and hypertension in IH-exposed rats. |
ChIP (HIF-1α binding at Nox4 HRE), KDM6B shRNA and GSK-J4 inhibitor in PC12 cells, in vivo IH rat model with blood pressure monitoring |
Physiological Genomics |
Medium |
34297635
|
| 2010 |
Jmjd3 is recruited to the proximal promoter of Mash1 via interaction with the transcription factor Hes1; Jmjd3 removes H3K27me3 at the Mash1 promoter to activate Mash1 expression during RA-induced neuronal differentiation of P19 cells; Co-IP confirms Jmjd3-Hes1 physical interaction. |
ChIP at Mash1 promoter, Co-IP of Jmjd3-Hes1, siRNA and dominant negative Jmjd3 mutant, overexpression in P19 cells, promoter-reporter assays |
Journal of Cellular Biochemistry |
High |
20506217
|
| 2018 |
JMJD3 mediates doxorubicin-induced cardiomyopathy by reducing H3K27me3 at the SESN2 promoter, thereby suppressing SESN2 expression and leading to mitochondrial dysfunction and cardiomyocyte apoptosis; overexpression of SESN2 rescues JMJD3-induced cardiomyopathy. |
ChIP at SESN2 promoter, JMJD3 KD/OE, SESN2 rescue overexpression, mitochondrial function assays, human dilated cardiomyopathy tissue analysis |
Frontiers in Cell and Developmental Biology |
Medium |
33117796
|
| 2018 |
Active KDM6B H3K27me3 demethylase activity is required for the global decrease in H3K27me3 between the 2-cell and 8-cell stages of bovine preimplantation development; KDM6B knockdown or catalytic inhibition prevents blastocyst formation, reduces ICM/TE cell numbers, and alters the embryonic transcriptome at the 8-cell stage. |
Maternal KDM6B mRNA knockdown in bovine embryos, catalytic inhibitor (KDM6B-specific), global H3K27me3 immunostaining, transcriptome analysis at 8-cell stage |
Epigenetics |
High |
29160132
|
| 2019 |
KDM6B epigenetically activates neuronal differentiation genes in neuroblastoma by removing H3K27me3; KDM6B functions downstream of the retinoic acid-HOXC9 axis; KDM6B is induced by retinoic acid via HOXC9, and KDM6B physically interacts with HOXC9 to target neuronal gene loci for epigenetic activation. |
ChIP at neuronal gene loci, KDM6B KD and OE, retinoic acid treatment, Co-IP of KDM6B-HOXC9, neuroblastoma cell differentiation assays |
Oncogenesis |
High |
30631055
|
| 2021 |
JMJD3 promotes TGF-β-induced EMT in Ras-activated lung cancer cells by epigenetically inducing syntenin expression through removal of H3K27me3 at the syntenin promoter; syntenin then regulates TGF-β receptor activation; JMJD3 expression is regulated by Ras activity. |
ChIP at syntenin promoter, Co-IP of JMJD3-syntenin, JMJD3 KD/OE, TGF-β-Smad activation assays, tissue array analysis |
Oncogenesis |
Medium |
33637682
|
| 2015 |
KDM6B directly interacts with FOXO1 in NSCLC cells; KDM6B overexpression promotes nuclear translocation/accumulation of FOXO1, initiating mitochondria-dependent apoptosis; KDM6B-induced apoptosis and anti-metastatic effects are abrogated by FOXO1 knockdown. |
Co-IP of KDM6B-FOXO1, nuclear fractionation, FOXO1 KD epistasis, apoptosis and invasion assays in NSCLC cells |
Cellular Physiology and Biochemistry |
Medium |
26303949
|
| 2021 |
The Notch-effector CSL directly represses KDM6B transcription in keratinocytes and SCC cells; increased CSL levels suppress KDM6B, enhancing proliferative potential; CSL silencing induces KDM6B, promoting growth arrest, apoptosis, and differentiation in SCC. |
Global transcriptomics of CSL-silenced HKCs and SCC cells, ChIP for CSL at KDM6B promoter (implied by direct target designation), in vivo SCC tumor models |
Journal of Clinical Investigation |
Medium |
29757189
|
| 2022 |
ERα is recruited to the KDM6B promoter upon estrogen stimulation, directly enhancing KDM6B expression; KDM6B is then recruited to BMP2 and HOXC6 promoters, removing H3K27me3 and activating osteogenic transcription; KDM6B depletion abolishes estrogen's pro-osteogenic effects in vivo. |
ChIP of ERα at KDM6B promoter and KDM6B at BMP2/HOXC6 promoters, KDM6B shRNA in DMSCs, in vivo calvarial bone regeneration model |
Bone Research |
High |
34992221
|
| 2017 |
Jmjd3, but not Utx, is required for axial skeletal patterning in mice; Jmjd3 mutant embryos display anterior homeotic transformation associated with reduced Hox gene expression; ChIP in embryonic tailbuds shows elevated H3K27me3 at Hox loci in Jmjd3 mutants; demethylase-inactive Jmjd3 mutants phenocopy the Jmjd3 knockout. |
Jmjd3 knockout and demethylase-inactive mutant mice, ChIP at Hox loci in tailbuds, microarray gene expression analysis |
FASEB Journal |
High |
28188179
|