HCSGD entry for KDM6B
1. General information
| Official gene symbol | KDM6B |
|---|---|
| Entrez ID | 23135 |
| Gene full name | lysine (K)-specific demethylase 6B |
| Other gene symbols | JMJD3 |
| Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
|---|---|---|---|
| GO:0005515 | Protein binding | IPI | molecular_function |
| GO:0005634 | Nucleus | IEA | cellular_component |
| GO:0006954 | Inflammatory response | IEA | biological_process |
| GO:0016577 | Histone demethylation | IEA | biological_process |
| GO:0043565 | Sequence-specific DNA binding | IEA | molecular_function |
| GO:0045944 | Positive regulation of transcription from RNA polymerase II promoter | IEA | biological_process |
| GO:0046872 | Metal ion binding | IEA | molecular_function |
| GO:0051213 | Dioxygenase activity | IEA | molecular_function |
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4. Expression levels in datasets
- Meta-analysis result
| p-value up | p-value down | FDR up | FDR down |
|---|---|---|---|
| 0.0202135177 | 0.9594591163 | 0.3423680824 | 1.0000000000 |
- Individual experiment result
( "-" represent NA in the specific microarray platform )
( "-" represent NA in the specific microarray platform )
| Data source | Up or down | Log fold change |
|---|---|---|
| GSE11954 | Down | -0.4884385842 |
| GSE13712_SHEAR | Down | -0.1499079778 |
| GSE13712_STATIC | Down | -0.0814539132 |
| GSE19018 | Down | -0.0427159327 |
| GSE19899_A1 | Up | 0.2296578654 |
| GSE19899_A2 | Up | 1.1515955658 |
| PubMed_21979375_A1 | Up | 0.8104290491 |
| PubMed_21979375_A2 | Up | 1.3688455922 |
| GSE35957 | Down | -0.1310016611 |
| GSE36640 | Up | 0.1212236062 |
| GSE54402 | Up | 0.4771437655 |
| GSE9593 | Down | -0.1253851269 |
| GSE43922 | Up | 0.8234034086 |
| GSE24585 | Up | 0.4019493687 |
| GSE37065 | Up | 0.0936522795 |
| GSE28863_A1 | Up | 0.1621206723 |
| GSE28863_A2 | Up | 0.0403584659 |
| GSE28863_A3 | Up | 0.3002624150 |
| GSE28863_A4 | Down | -0.0128127370 |
| GSE48662 | Up | 0.3190831066 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
Not regulated by compounds
- Drugs
Not regulated by drugs
- MicroRNAs
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
|---|---|---|---|---|---|
| hsa-miR-335-5p | MIMAT0000765 | MIRT017568 | Microarray | Functional MTI (Weak) | 18185580 |
| hsa-miR-186-5p | MIMAT0000456 | MIRT021179 | Sequencing | Functional MTI (Weak) | 20371350 |
| hsa-miR-101-3p | MIMAT0000099 | MIRT027296 | Sequencing | Functional MTI (Weak) | 20371350 |
| hsa-miR-18a-3p | MIMAT0002891 | MIRT040965 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-92a-3p | MIMAT0000092 | MIRT049017 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-let-7a-5p | MIMAT0000062 | MIRT052574 | CLASH | Functional MTI (Weak) | 23622248 |
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- mirRecord
No target information from mirRecord
6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 12 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
|---|---|
| 27114850 | HIF-1alpha stimulates the expression of KDM3A, KDM4B, KDM4C, and KDM6B, which enhance gene transcription by demethylating H3K9 and H3K27 sites (repressive epigenetic marks) |
| 26957416 | Histone demethylase JMJD3 at the intersection of cellular senescence and cancer |
| 26957416 | Histone modifications and chromatin remodeling related to the function of a histone demethylase, jumonji domain-containing protein 3 (JMJD3; also known as KDM6B), play an important role in development, tissue regeneration, stem cells, inflammation, and cellular senescence and aging |
| 26957416 | The role of JMJD3 in cancer is poorly understood and its function may be at the intersection of many pathways promoted in a dysfunctional manner such as activation of the senescence-associated secretory phenotype (SASP) observed in aging |
| 25698448 | JMJD3 promotes SAHF formation in senescent WI38 cells by triggering an interplay between demethylation and phosphorylation of RB protein |
| 25698448 | Here we report that JMJD3, a histone demethylase catalyzing the tri-methylation of H3K27 (H3K27me3), can demethylate the non-histone protein RB at the lysine810 residue (K810), which is a target of the methyltransferase Set7/9 |
| 25698448 | Furthermore, during the process of SAHF assembly, JMJD3 was transported to the cytoplasm and interacted with RB through its demethylase domain JmjC |
| 25698448 | This study highlights the role of JMJD3 as a novel inducer of SAHF formation through demethylating RB and provides new insights into the mechanisms of cellular senescence and SAHF assembly |
| 25652587 | UNLABELLED: Jumonji domain-containing protein 3 (JMJD3/KDM6B) demethylates lysine 27 on histone H3 (H3K27me3), a repressive epigenetic mark controlling chromatin organization and cellular senescence |
| 25652587 | To better understand the functional consequences of JMJD3 its expression was investigated in brain tumor cells |
| 25652587 | Querying patient expression profile databases confirmed JMJD3 overexpression in high-grade glioma |
| 25652587 | Overexpressing wild-type JMJD3 (JMJD3wt) activated SASP-associated genes, enhanced SA-beta-gal activity, and induced nuclear blebbing |
| 25652587 | Conversely, overexpression of a catalytically inactive dominant negative mutant JMJD3 (JMJD3mut) increased proliferation |
| 25652587 | IMPLICATIONS: This glioma study brings together actions of a normal epigenetic mechanism (JMJD3 activity) with dysfunctional activation of senescence-related processes, including secretion of SASP proinflammatory cytokines and stem cell tropism toward tumors |
| 24925089 | Histone demethylase Jumonji D3 (JMJD3/KDM6B) at the nexus of epigenetic regulation of inflammation and the aging process |
| 24925089 | Jumonji domain-containing protein 3 (JMJD3), also called lysine-specific demethylase 6B (KDM6b), is an inducible histone demethylase which enhances immune responses and can trigger cellular senescence |
| 24925089 | JMJD3 potentiates gene expression by demethylating repressive H3K27me3 epigenetic marks in promoters and gene bodies |
| 24925089 | Moreover, JMJD3 also stimulates transcription in a demethylase-independent manner by mediating interactions between chromatin modifiers |
| 24925089 | JMJD3 can enhance both pro-inflammatory and anti-inflammatory responses by targeting distinct transcription factors in a context-dependent manner in gene promoters |
| 24925089 | For instance, JMJD3 can induce macrophage M2 polarization via STAT6 signaling |
| 24925089 | JMJD3 also interacts with T-bet factor and induces Th1 differentiation of CD4(+) T cells |
| 24925089 | Moreover, JMJD3 can activate TGF-beta signaling through the SMAD3 pathway |
| 24925089 | Conversely, JMJD3 displaces polycomb complexes from the INK4 box, which induces the expression of INK4a and triggers cellular senescence |
| 24925089 | JMJD3 can also enhance the nuclear localization of p53 and thus regulate its function |
| 24925089 | We will briefly review the inducible properties of JMJD3 expression and then focus on the role of JMJD3 in the regulation of inflammation and senescence through different signaling pathways |
| 24925089 | We emphasize that an inflammatory milieu and cellular stress can enhance immune responses and provoke cellular senescence via epigenetic regulation through JMJD3 activation |
| 24797517 | The histone lysine demethylase JMJD3/KDM6B is recruited to p53 bound promoters and enhancer elements in a p53 dependent manner |
| 24797517 | The JmjC domain-containing protein JMJD3/KDM6B catalyses the demethylation of H3K27me3 and H3K27me2 |
| 24797517 | JMJD3 appears to be highly regulated at the transcriptional level and is upregulated in response to diverse stimuli such as differentiation inducers and stress signals |
| 24797517 | Accordingly, JMJD3 has been linked to the regulation of different biological processes such as differentiation of embryonic stem cells, inflammatory responses in macrophages, and induction of cellular senescence via regulation of the INK4A-ARF locus |
| 24797517 | Here we show here that JMJD3 interacts with the tumour suppressor protein p53 |
| 24797517 | Following DNA damage, JMJD3 is transcriptionally upregulated and by performing genome-wide mapping of JMJD3, we demonstrate that it binds genes involved in basic cellular processes, as well as genes regulating cell cycle, response to stress and apoptosis |
| 24797517 | Moreover, we find that JMJD3 binding sites show significant overlap with p53 bound promoters and enhancer elements |
| 24797517 | The binding of JMJD3 to p53 target sites is increased in response to DNA damage, and we demonstrate that the recruitment of JMJD3 to these sites is dependent on p53 expression |
| 24797517 | Therefore, we propose a model in which JMJD3 is recruited to p53 responsive elements via its interaction with p53 and speculate that JMJD3 could act as a fail-safe mechanism to remove low levels of H3K27me3 and H3K27me2 to allow for efficient acetylation of H3K27 |
| 24046371 | Induction of p16(INK4A) expression is not a consequence of retinoblastoma tumor suppressor inactivation but is triggered by a cellular senescence response and is mediated by epigenetic derepression through the H3K27-specific demethylase (KDM)6B |
| 24046371 | HPV E7 expression causes an acute dependence on KDM6B expression for cell survival |
| 24046371 | The p16(INK4A) tumor suppressor is a critical KDM6B downstream transcriptional target and its expression is critical for cell survival |
| 22020331 | Here, we present evidence that loss of BTG3 in normal cells induced cellular senescence, which was correlated with enhanced ERK-AP1 signaling and elevated expression of the histone H3K27me3 demethylase JMJD3/KDM6B, leading to acute induction of p16(INK4a) |
| 21518927 | Up-regulation of the histone-demethylase Jmjd3 and de-methylation at the p16INK4a promoter contributed to the effect of NPM-ALK on p16INK4a, which was transcriptionally regulated |
| 20049504 | Decreased expression of histone deacetylases (HDACs), followed by downregulation of polycomb group genes (PcGs), such as BMI1, EZH2 and SUZ12, and by upregulation of jumonji domain containing 3 (JMJD3), was observed in senescent MSCs |
| 20049504 | Similarly, HDAC inhibitors induced cellular senescence through downregulation of PcGs and upregulation of JMJD3 |
| 20049504 | JMJD3 expression regulation was dependant on histone acetylation status at its promoter regions |
| 20049504 | These results suggest that HDAC activity might be important for MSC self-renewal by balancing PcGs and JMJD3 expression, which govern cellular senescence by p16(INK4A) regulation |
| 19451218 | Histone demethylase JMJD3 contributes to epigenetic control of INK4a/ARF by oncogenic RAS |
| 19451218 | Here we show that signaling from oncogenic RAS overrides PcG-mediated repression of INK4a by activating the H3K27 demethylase JMJD3 and down-regulating the methyltransferase EZH2 |
| 19451218 | In human fibroblasts, JMJD3 activates INK4a, but not ARF, and causes p16(INK4a)-dependent arrest |
| 19451218 | In mouse embryo fibroblasts, Jmjd3 activates both Ink4a and Arf and elicits a p53-dependent arrest, echoing the effects of RAS in this system |
| 19451218 | Our findings directly implicate JMJD3 in the regulation of INK4a/ARF during oncogene-induced senescence and suggest that JMJD3 has the capacity to act as a tumor suppressor |
| 19451217 | The H3K27me3 demethylase JMJD3 contributes to the activation of the INK4A-ARF locus in response to oncogene- and stress-induced senescence |
| 19451217 | Here, we show that expression of the histone H3 Lys 27 (H3K27) demethylase JMJD3 is induced upon activation of the RAS-RAF signaling pathway |
| 19451217 | JMJD3 is recruited to the INK4A-ARF locus and contributes to the transcriptional activation of p16INK4A in human diploid fibroblasts |
| 19451217 | Additionally, inhibition of Jmjd3 expression in mouse embryonic fibroblasts results in suppression of p16Ink4a and p19Arf expression and in their immortalization |
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