| 2007 |
Jmjd1a (KDM3A) demethylates H3K9me2 at the promoter regions of Tcl1, Tcfcp2l1, and Zfp57 in mouse embryonic stem cells, positively regulating the expression of these pluripotency-associated genes. Jmjd1a depletion leads to ES cell differentiation accompanied by reduction of ES cell-specific gene expression. |
RNAi knockdown, ChIP assay, gene expression analysis |
Genes & development |
High |
17938240
|
| 2008 |
HIF-1α binds to specific hypoxia-response elements (HREs) in the JMJD1A gene promoter and directly induces JMJD1A expression under hypoxia. JMJD1A protein retains H3K9 demethylase activity under hypoxic conditions. |
ChIP assay identifying HIF-1α binding to JMJD1A promoter HRE; siRNA knockdown of HIF-1 abolishing hypoxia-induced JMJD1A upregulation; in vitro demethylase activity assay |
The Journal of biological chemistry |
High |
18538129 18984585
|
| 2009 |
Nickel ions inhibit KDM3A demethylase activity by replacing the catalytic Fe(II) at the active site. Without iron, ~1 molecule of Ni(II) inhibits 1 molecule of KDM3A (IC50 ~2.5 µM). Nickel-bound KDM3A cannot be reactivated by excess iron. Nickel also inhibits KDM3A in intact cells. |
In vitro demethylase activity assay with varying Ni/Fe concentrations; X-ray absorption spectroscopy on ABH2 showing Ni binds same site as Fe; cell-based inhibition assays |
The Journal of biological chemistry |
High |
20042601
|
| 2012 |
KDM3A is recruited to the SLC2A3 (GLUT3) locus in a HIF-1-dependent manner and demethylates H3K9me2 at this locus, facilitating chromatin looping and upregulating GLUT3 expression under hypoxia. Knockdown of both HIF-1α and KDM3A suppresses hypoxia-induced glycolytic gene expression. |
ChIP-seq, ChIP assay, 3C (chromatin conformation capture), RNAi knockdown, DNA microarray |
Molecular and cellular biology |
High |
22645302
|
| 2013 |
Jmjd1a directly binds to the Sry gene locus and regulates H3K9me2 marks there, positively controlling Sry expression. Loss of Jmjd1a leads to male-to-female sex reversal in mice due to insufficient Sry expression. |
Jmjd1a knockout mouse model, ChIP assay at Sry locus, gene expression analysis |
Science |
High |
24009392
|
| 2013 |
KDM3A forms a complex with KSHV LANA protein in the nucleus. This complex demethylates H3K9me2 at LANA recruitment sites on the KSHV episome, maintaining H3K9 hypomethylation at immediate-early and latent gene promoters and supporting viral gene expression and replication. H3K9 methylation inhibits LANA binding to the H3 tail. |
Co-immunoprecipitation from nuclear extracts, pulldown with purified proteins, ChIP with KSHV tiling arrays, KDM3A knockdown |
Journal of virology |
High |
23576503
|
| 2013 |
KDM3A demethylates H3K9me2 at the promoter of HOXA1 and activates its transcription, promoting G1/S cell cycle progression. KDM3A siRNA reduces HOXA1 and CCND1 expression, resulting in G1 arrest in cancer cells. |
ChIP assay showing KDM3A binding and H3K9me2 demethylation at HOXA1 promoter; siRNA knockdown with cell cycle analysis |
International journal of cancer |
Medium |
22020899
|
| 2013 |
JMJD1A binds to the MALAT1 gene promoter and demethylates histone H3K9, thereby upregulating MALAT1 expression, which in turn promotes neuroblastoma cell migration and invasion. N-Myc activates JMJD1A expression by binding the JMJD1A promoter. |
ChIP assay, RT-PCR, Affymetrix microarray, cell migration/invasion assays, JMJD1A inhibitor treatment |
Oncotarget |
Medium |
24742640
|
| 2014 |
KDM3A is a positive regulator of estrogen receptor (ER) activity in breast cancer. KDM3A depletion abrogates ER recruitment to cis-regulatory elements at target gene promoters and inhibits estrogen-induced gene expression. Catalytic demethylase activity of KDM3A is required for ER-target gene expression and cell growth. |
RNAi knockdown, ChIP assay, global gene expression analysis, catalytic mutant rescue experiments |
Nucleic acids research |
High |
25488809
|
| 2014 |
ACK1 tyrosine kinase phosphorylates KDM3A at tyrosine 1114 (Y1114) in a heregulin-dependent manner. This phosphorylation enhances KDM3A demethylase activity, decreasing H3K9me2 marks and increasing transcription of the ER co-regulated gene HOXA1 even in the presence of tamoxifen. |
In vitro kinase assay, phospho-site mapping, ChIP assay, ACK1 knockdown/inhibitor treatment, mutational analysis |
The Journal of biological chemistry |
High |
25148682
|
| 2014 |
Kdm3a localizes to cytoplasmic structures in maturing spermatids (acrosome, manchette) in addition to its nuclear role. Kdm3a protein stability, subcellular distribution, and demethylase activity are dependent on Hsp90, identifying it as an Hsp90 client. Loss of Kdm3a demethylase activity causes abnormal acrosome, manchette, and absence of implantation fossa, affecting cytoskeletal components β-actin and γ-tubulin fractionation. |
Electron microscopy, cellular fractionation, Hsp90 inhibitor treatment, two Kdm3a mouse models (demethylase activity mutant), immunolocalization |
Molecular biology of the cell |
High |
24554764
|
| 2015 |
JMJD1A is phosphorylated at serine 265 (S265) by protein kinase A (PKA) downstream of β-adrenergic signaling. This phosphorylation promotes JMJD1A interaction with the SWI/SNF nucleosome remodelling complex and DNA-bound PPARγ, facilitating long-range chromatin interactions and rapid target gene activation (Adrb1, Ucp1) in brown adipocytes. The S265 phosphorylation-dependent chromatin scaffold function is independent of demethylase activity, while H3K9me2 demethylation is a separate function required for sustained gene activation. |
PKA phosphorylation assay, Co-IP of JMJD1A with SWI/SNF and PPARγ, ChIP, chromatin conformation capture, S265A mutant rescue experiments |
Nature communications |
High |
25948511
|
| 2015 |
JMJD1A promotes c-Myc transcriptional activation by enhancing androgen receptor (AR) recruitment to the c-Myc gene enhancer and inducing H3K9 demethylation, increasing AR-dependent c-Myc mRNA. In parallel, JMJD1A (including catalytically inactive mutant) binds HUWE1 E3 ubiquitin ligase, attenuating HUWE1-dependent ubiquitination and degradation of c-Myc protein. |
ChIP assay, Co-IP (JMJD1A-HUWE1), ubiquitination assay, catalytic mutant analysis, knockdown/rescue experiments |
Oncogene |
High |
26279298
|
| 2015 |
JMJD1A demethylates H3K9me2 at the PPARγ gene promoter in hepatic stellate cells, maintaining PPARγ expression and restraining fibrosis. JMJD1A knockdown reinforces H3K9me2 at the PPARγ promoter and increases fibrosis markers; overexpression of wild-type but not catalytically inactive JMJD1A rescues the phenotype. |
ChIP assay, siRNA/shRNA knockdown, wild-type vs. catalytic mutant overexpression, in vivo mouse liver fibrosis model |
FASEB journal |
High |
25609425
|
| 2016 |
KDM3A maintains expression of KLF2 and IRF4 in multiple myeloma cells through H3K9 demethylation at their loci. KDM3A, KLF2, and IRF4 form a survival axis where KLF2 directly activates IRF4 and IRF4 reciprocally upregulates KLF2. KDM3A/KLF2/IRF4 knockdown also decreases ITGB7 expression, reducing MM cell adhesion to bone marrow stromal cells and homing. |
ChIP assay showing H3K9 demethylation at KLF2/IRF4 loci, siRNA knockdown (in vitro and in vivo xenograft), luciferase reporter assay for KLF2→IRF4 axis |
Nature communications |
High |
26728187
|
| 2016 |
KDM3A demethylates non-histone substrate p53 at monomethylated K372 (p53-K372me1), suppressing p53's pro-apoptotic function. KDM3A also demethylates H3K9 to promote pro-invasive gene transcription. Depletion of KDM3A can reactivate mutant p53 to induce pro-apoptotic gene expression. |
Co-IP, in vitro demethylation assay on p53-K372me1 peptide, ChIP, RNAi knockdown, gene expression analysis |
Oncogene |
High |
27270439
|
| 2016 |
Normal ECM mechanosensing triggers downregulation and nuclear exit of JMJD1A in carcinoma cells, resulting in epigenetic growth restriction. JMJD1A positively regulates transcription of multiple target genes including YAP/TAZ in a matrix-stiffness-dependent manner. |
JMJD1A knockdown and localization studies, cell growth assays on different ECM stiffness, gene expression profiling |
Nature communications |
Medium |
27488962
|
| 2016 |
KDM3A directly demethylates H3K9me2 at the MCAM promoter and also regulates MCAM expression indirectly via the Ets1 transcription factor, promoting Ewing Sarcoma cell migration and metastasis. |
ChIP assay at MCAM promoter, RNAi knockdown, in vitro migration assay, in vivo experimental metastasis model |
Oncogene |
High |
28319067
|
| 2013 |
Control of H3K9 methylation state by JMJD1A homodimerization: JMJD1A forms a homodimer through its catalytic domains, placing two active sites in proximity. This enables substrate channeling—efficient conversion of H3K9me2 to unmethylated H3K9 by reducing release of the monomethylated intermediate. Inactivating one active site in the dimer significantly reduces demethylation rate without changing affinity for the intermediate. |
In vitro demethylation assay, size-exclusion chromatography/native gel demonstrating homodimerization, heterodimer (WT + inactive mutant) enzymatic analysis |
The Journal of biological chemistry |
High |
24214985
|
| 2017 |
JMJD1A (KDM3A) promotes alternative splicing of AR-V7 through heterogeneous nuclear ribonucleoprotein F (HNRNPF). JMJD1A interacts with HNRNPF and promotes its recruitment to a cryptic exon 3b on AR pre-mRNA. Knockdown of JMJD1A or HNRNPF inhibits AR-V7 splicing but not full-length AR in a minigene reporter assay. |
Co-IP (JMJD1A-HNRNPF), RIP (RNA immunoprecipitation), minigene reporter assay, siRNA knockdown |
Proceedings of the National Academy of Sciences |
High |
29712835
|
| 2017 |
KDM3A is recruited to the promoter of glycolytic gene PGK1, demethylates H3K9me2, and cooperates with HIF1α to induce glycolytic gene expression. A catalytically inactive JMJD1A mutant (H1120Y) fails to demethylate H3K9me2 at the PGK1 promoter and fails to cooperate with HIF1α, establishing that demethylase activity is required for HIF1α coactivation. |
ChIP assay at PGK1 promoter, catalytic mutant (H1120Y) analysis, siRNA knockdown, cell proliferation/colony formation assays |
Oncogene |
High |
28263974
|
| 2017 |
KDM3A promotes tumorigenesis in the PI3K-activated liver by recruiting c-Jun to AP-1 binding sites of target genes (Cd44, Mmp7, Pdgfrb) and facilitating Brg1 (SWI/SNF component) binding, in a Kdm3a-dependent manner, without affecting c-Jun expression. Loss of Kdm3a attenuates tumor formation in Pik3ca transgenic mice. |
ChIP assay showing KDM3A, c-Jun, and Brg1 binding at AP-1 sites, Kdm3a knockout in Pik3ca transgenic mice, transcriptome analysis |
Oncogene |
High |
28692045
|
| 2017 |
KDM3A coordinates cilia stability by regulating actin gene expression (nuclear function) and by directly binding to the actin cytoskeleton (non-nuclear function), creating an 'actin gate' involving ARP2/3 activity that controls IFT protein recruitment into cilia. Loss of KDM3A causes abnormally wide range of cilia lengths, delayed disassembly, and accumulation of IFT proteins. Promoting actin filament formation rescues KDM3A mutant ciliary defects. |
KDM3A knockout mouse model (phenocopying ciliopathy), actin cytoskeleton binding assay, IFT protein accumulation imaging, ARP2/3 inhibitor rescue, actin depolymerization mimicry experiments |
The Journal of cell biology |
High |
28246120
|
| 2018 |
KDM3A is tyrosine-phosphorylated by JAK2 in the nucleus and functions as a STAT3-dependent transcriptional coactivator. JAK2-mediated KDM3A phosphorylation induced by IL-6 alters histone H3K9 methylation as the predominant epigenetic event in JAK2-STAT3 pathway activation. |
In vitro kinase assay (JAK2 phosphorylating KDM3A), Co-IP, ChIP showing H3K9 methylation changes, cell-based IL-6 stimulation experiments |
Proceedings of the National Academy of Sciences |
High |
30377265
|
| 2018 |
JMJD1A coordinates acute and chronic cold adaptation through two mechanisms requiring S265 phosphorylation by PKA: (1) phosphorylation-dependent but demethylation-independent acute Ucp1 induction in BAT via long-range chromatin interactions; (2) phosphorylation plus H3K9me2 demethylation for chronic Ucp1 expression in beige subcutaneous WAT via a PRDM16-PPARγ-P-JMJD1A complex. |
S265A phospho-mutant mouse model, ChIP, chromatin conformation capture, Co-IP of JMJD1A-PRDM16-PPARγ complex, cold exposure experiments |
Nature communications |
High |
29674659
|
| 2019 |
KDM3A binds PGC-1α and demethylates monomethylated K224 of PGC-1α (a non-histone substrate) under normoxic conditions. Hypoxia inhibits KDM3A (which has high KM for oxygen), causing accumulation of PGC-1α K224 monomethylation that decreases PGC-1α activity for NRF1/NRF2-dependent transcription of TFAM, TFB1M, TFB2M, reducing mitochondrial biogenesis. PGC-1α K224R mutant significantly increases mitochondrial biogenesis and tumor cell apoptosis. |
Co-IP (KDM3A-PGC-1α), in vitro demethylation assay on PGC-1α K224me1, oxygen-dependent activity assay, PGC-1α K224R mutant in cells and brain tumor xenograft model |
Molecular cell |
High |
31629659
|
| 2019 |
PHF5A acetylation at K29 (by p300 in response to nutrient stress) strengthens U2 snRNP interactions and induces alternative splicing that stabilizes KDM3A mRNA, increasing KDM3A protein expression. This PHF5A acetylation → KDM3A upregulation axis promotes colorectal cancer stress resistance. |
Proteomics identifying PHF5A hyperacetylation, Co-IP (PHF5A-U2 snRNP components), splicing reporter assay, RNA-seq, KDM3A rescue experiments |
Molecular cell |
High |
31054974
|
| 2019 |
KDM3A binds to the DCLK1 promoter and activates DCLK1 expression. KDM3A knockdown reduces DCLK1 levels in pancreatic cancer cells; overexpression of KDM3A in normal pancreatic ductal cells enables tumor and metastasis formation in vivo. |
ChIP identifying KDM3A binding sites at DCLK1 promoter, siRNA knockdown, KDM3A overexpression in HPNE cells, orthotopic xenograft model |
Gastroenterology |
High |
31442435
|
| 2019 |
KDM3A demethylates H3K9me2 at enhancers of hippo pathway target genes and promotes H3K27ac deposition there. KDM3A associates with p300 and is required for p300 recruitment to enhancers. KDM3A depletion causes H3K9me2 accumulation mainly at TEAD1-binding enhancers, reducing TEAD1 binding and impairing transcription. KDM3A also upregulates YAP1 expression. |
ChIP-seq (H3K9me2, H3K27ac, H3K4me3), Co-IP (KDM3A-p300), siRNA knockdown, YAP1 rescue experiments |
Nucleic acids research |
High |
30649550
|
| 2019 |
KDM3A and KDM4C regulate heterochromatin reorganization during MSC senescence by transcriptionally activating condensin components NCAPD2 and NCAPG2 through H3K9 demethylation. Kdm3a-/- mouse MSCs exhibit defective chromosome organization and exacerbated DNA damage response, associated with accelerated bone aging. |
KDM3A/KDM4C knockdown and Kdm3a-/- mouse model, ChIP assay at condensin gene promoters, DNA damage response assays |
iScience |
Medium |
31704649
|
| 2020 |
JMJD1A protein stability is regulated by the E3 ubiquitin ligase STUB1, which mediates JMJD1A degradation. The acetyltransferase p300 acetylates JMJD1A at lysine 421 (K421), recruiting BRD4 to block STUB1-mediated degradation and promoting JMJD1A recruitment to AR target sites. Additionally, HUWE1 induces K27-/K29-linked noncanonical ubiquitination of JMJD1A at lysine-918. |
Co-IP (JMJD1A-STUB1, JMJD1A-p300, JMJD1A-BRD4), ubiquitination assay, acetylation mapping (K421), ChIP, CRPC clinical specimen correlation |
Cancer research |
High |
32238799 32522824
|
| 2020 |
KDM3A regulates alternative splicing of cell-cycle genes following DNA damage. KDM3A undergoes PKA-mediated phosphorylation at S265 upon DNA damage, which is required for proper cell-cycle regulation. KDM3A regulates SAT1 alternative splicing through a demethylase-independent mechanism requiring its interaction with ARID1A (SWI/SNF subunit) and SRSF3 splicing factor; KDM3A is essential for SRSF3 binding to SAT1 pre-mRNA. |
RNA-seq, Co-IP (KDM3A-ARID1A, KDM3A-SRSF3), phosphorylation assay at S265, catalytic mutant analysis, RIP (SRSF3 on SAT1 pre-mRNA) |
RNA |
High |
34321328
|
| 2021 |
KDM3A and KDM3B form a complex (demonstrated by IP-MS) that performs H3K9 demethylation cooperatively. OCT4 and SOX2 co-operate with the KDM3A/KDM3B-containing complex to maintain H3K9 hypomethylation at pluripotency gene loci and sustain the pluripotency gene regulatory network in porcine iPSCs. |
IP-mass spectrometry (KDM3A-KDM3B complex), ChIP-seq (H3K9me2/me3), co-depletion of KDM3A and KDM3B, gene expression analysis |
FASEB journal |
Medium |
34042215
|
| 2021 |
MDFI and MDFIC proteins interact with JMJD1A. JMJD1A influences transcription of several genes co-regulated by MDFI or MDFIC, including the HIC1 tumor suppressor gene which is co-stimulated by JMJD1A and MDFIC. Catalytically inactive JMJD1A mutant does not cooperate with ETV1 to induce MMP1, establishing demethylase requirement for this co-activation. |
Co-IP (JMJD1A-MDFI/MDFIC), RNA-seq, luciferase reporter with JMJD1A catalytic mutant, gene expression analysis |
Scientific reports |
Medium |
32457453
|
| 2016 |
KDM3A promotes anoikis in epithelial cells following matrix detachment by transcriptionally activating BNIP3 and BNIP3L via H3K9 demethylation. Integrin signaling in attached cells maintains low KDM3A expression; upon detachment, reduced integrin signaling increases KDM3A expression. KDM3A knockdown substantially reduces apoptosis following detachment; KDM3A ectopic expression induces cell death in attached cells. |
RNAi screen identifying KDM3A, ChIP assay at BNIP3/BNIP3L promoters, ectopic KDM3A expression, mouse breast cancer metastasis model |
eLife |
High |
27472901
|
| 2016 |
In hypoxic myeloma cells, the HIF-1α→KDM3A→MALAT1 axis promotes antiapoptotic phenotype independent of IRF4. KDM3A expression is HIF-1α-dependent, and KDM3A knockdown induces myeloma cell apoptosis under chronic hypoxia, while knockdown increases H3K9 methylation at MALAT1 locus. |
siRNA knockdown, ChIP at MALAT1 locus, gene expression analysis, apoptosis assays under chronic hypoxia |
Blood advances |
Medium |
29444873
|
| 2017 |
JMJD1A promotes Snail transcriptional activation by directly binding to the Snail gene promoter and demethylating H3K9me1 and H3K9me2 at its specific promoter region, thereby promoting prostate cancer progression. |
ChIP assay at Snail promoter, Co-IP (JMJD1A-Snail gene complex), siRNA knockdown, ectopic expression, xenograft model |
Molecular cancer research |
Medium |
32019811
|
| 2018 |
JMJD1A promotes β-catenin expression, interacts with β-catenin to enhance its transactivation, and demethylates H3K9me2 at c-Myc and MMP9 gene promoters to activate Wnt/β-catenin target genes. A catalytic mutant (H1120Y) fails to demethylate H3K9me2 at these promoters and fails to promote CRC progression, establishing demethylase activity requirement. |
ChIP assay at c-Myc and MMP9 promoters, Co-IP (JMJD1A-β-catenin), H1120Y catalytic mutant analysis, xenograft tumor model |
The Journal of biological chemistry |
High |
29802196
|
| 2023 |
JMJD1A is a major iron-dependent epigenetic enzyme for adipocyte differentiation, demethylating H3K9me2 at Pparg and other adipogenesis gene loci. Iron supply through lysosome-mediated ferritinophagy is crucial for JMJD1A activity during early adipocyte differentiation; iron deficiency suppresses H3K9me2 demethylation and blocks terminal differentiation. |
JMJD1A knockdown, ChIP-seq (H3K9me2), iron chelation/ferritinophagy inhibition, mass spectrometry of histone marks, integrated genome-wide analysis |
Nucleic acids research |
High |
37158274
|
| 2024 |
JMJD1A mediates β-adrenergic-induced H3K9 demethylation at Pgc1a/b enhancers in subcutaneous white adipose tissue (scWAT), promoting PGC-1α/β-dependent mitochondrial biogenesis and beige adipocyte formation. Disruption of JMJD1A demethylase activity in mice impairs Pgc1a/b activation in scWAT and causes obesity, insulin resistance, and metabolic disorders, whereas JMJD1A demethylase activity is dispensable for BAT thermogenesis during acute cold stress. |
JMJD1A demethylase-activity mutant knock-in mice, ChIP at Pgc1a/b enhancers, β-adrenergic stimulation, metabolic phenotyping |
iScience |
High |
38544573
|
| 2006 |
TSGA/Jmjd1a (KDM3A) is a nuclear protein that contains functional transcription repression domains and interacts with the ETS transcription factor ER71 both in vitro and in vivo via its N-terminus (TSGA) and ER71's C-terminus. TSGA impairs ER71-mediated transcriptional activation from the MMP-1 promoter. |
GST pulldown, co-immunoprecipitation, reporter gene assay, immunostaining |
Journal of cellular biochemistry |
Medium |
16619273
|
| 2017 |
KDM3A regulates H3K9me2 at the proximal promoter regions of AGTR1 and ROCK2 to control their transcription, mediating the Rho/ROCK and AngII/AGTR1 signaling pathways in vascular smooth muscle cells. KDM3A overexpression accelerates while knockdown reduces neointima formation after carotid artery balloon injury in diabetic rats. |
ChIP assay at AGTR1 and ROCK2 promoters, adenoviral KDM3A overexpression and lentiviral siRNA knockdown in vivo and in vitro, rat carotid artery injury model |
Atherosclerosis |
Medium |
28135625
|
| 2019 |
KDM3A activates the JMJD1A-mediated demethylation of H3K9me2 at Erk2 and Klf2 promoters in bone marrow MSCs, elevating their expression and promoting osteogenic differentiation. |
ChIP assay at Erk2 and Klf2 promoters, miR-199a-3p targeting of KDM3A (dual-luciferase), overexpression and knockdown in MSCs |
The Biochemical journal |
Medium |
33410908
|
| 2018 |
JMJD1A and JMJD1B preferentially target H3K9 demethylation in gene-dense euchromatic regions of chromosomes, establishing global H3K9 hypomethylation in euchromatin. G9a-mediated H3K9 overmethylation is the direct cause of cell death and perturbed gene expression in JMJD1A/JMJD1B-depleted ESCs, established by epistasis using G9a heterozygous mutation or chemical inhibitor rescue. |
Double knockout ESCs and embryos, ChIP-seq (H3K9me1/me2), G9a heterozygous rescue, G9a inhibitor rescue |
Stem cell reports |
High |
29526734
|
| 2017 |
The GLP/G9a H3K9 methyltransferase complex catalyzes H3K9 methylation at the Sry locus. Heterozygous GLP mutation or chemical GLP/G9a inhibitor rescues sex-reversal in Jmjd1a-deficient mice by restoring Sry expression, demonstrating that Jmjd1a/KDM3A and GLP/G9a form a methylation-demethylation balance at the Sry locus. |
Genetic epistasis (Jmjd1a KO × Glp heterozygous mice), GLP/G9a chemical inhibitor treatment in Jmjd1a-deficient embryos, ChIP assay at Sry locus |
PLoS genetics |
High |
28949961
|
| 2017 |
Vitamin C specifically induces rapid, reversible demethylation of H3K9me2 (but not other histone methylation marks) in naïve embryonic stem cells via Kdm3a and Kdm3b. Kdm3a and Kdm3b are required for vitamin C-induced H3K9me2 demethylation at chromosomal domains, gene promoters, and repeat elements. This H3K9me2 demethylation is independent of Tet-mediated DNA demethylation at specific loci. |
Western blot, immunofluorescence, mass spectrometry of histone marks, ChIP-seq, Kdm3a/Kdm3b knockdown, epistasis with Tet enzyme inhibition |
Epigenetics & chromatin |
High |
28706564
|
| 2022 |
KDM3A binds to the ETS1 promoter and removes H3K9me2 to promote ETS1 transcription, protecting against myocardial I/R injury. KDM3A knockout exacerbates cardiac dysfunction, mitochondrial apoptosis, ROS, and inflammation both in vivo and in vitro. |
ChIP-PCR at ETS1 promoter, KDM3A knockout/overexpression (in vitro and rat in vivo I/R model), H3K9me2 demethylation assay |
Communications biology |
Medium |
35338235
|
| 2021 |
KDM3A activates DCLK1 expression by demethylating H3K9me2 at its promoter; DCLK1 in turn suppresses FXYD3 expression. Let-7i targets and downregulates KDM3A mRNA, reversing this axis in lung cancer cells. |
ChIP assay at DCLK1 promoter, dual-luciferase reporter (let-7i targeting KDM3A 3'UTR), siRNA knockdown, xenograft model |
Journal of cellular and molecular medicine |
Medium |
33350586
|
| 2023 |
NUPR1 promotes TFEB transcription in hypoxic glioma cells by binding to KDM3A, which reduces H3K9me2 levels at the TFEB promoter, thereby augmenting autophagy and TMZ resistance. |
Co-IP (NUPR1-KDM3A interaction), ChIP at TFEB promoter (KDM3A binding and H3K9me2 levels), siRNA knockdown, xenograft model |
Oncology research |
Medium |
37305393
|