HCSGD entry for EZH2
1. General information
| Official gene symbol | EZH2 |
|---|---|
| Entrez ID | 2146 |
| Gene full name | enhancer of zeste homolog 2 (Drosophila) |
| Other gene symbols | ENX-1 ENX1 EZH1 KMT6 KMT6A WVS WVS2 |
| Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
|---|---|---|---|
| GO:0000122 | Negative regulation of transcription from RNA polymerase II promoter | IDA | biological_process |
| GO:0001047 | Core promoter binding | IEA | molecular_function |
| GO:0003677 | DNA binding | TAS | molecular_function |
| GO:0003682 | Chromatin binding | IDA IEA | molecular_function |
| GO:0003723 | RNA binding | IEA | molecular_function |
| GO:0005515 | Protein binding | IPI | molecular_function |
| GO:0005737 | Cytoplasm | IEA | cellular_component |
| GO:0006325 | Chromatin organization | TAS | biological_process |
| GO:0006351 | Transcription, DNA-templated | IEA | biological_process |
| GO:0006355 | Regulation of transcription, DNA-templated | TAS | biological_process |
| GO:0010718 | Positive regulation of epithelial to mesenchymal transition | IDA | biological_process |
| GO:0014013 | Regulation of gliogenesis | IEA | biological_process |
| GO:0018024 | Histone-lysine N-methyltransferase activity | IEA | molecular_function |
| GO:0021695 | Cerebellar cortex development | IEA | biological_process |
| GO:0032320 | Positive regulation of Ras GTPase activity | IDA | biological_process |
| GO:0034244 | Negative regulation of transcription elongation from RNA polymerase II promoter | IEA | biological_process |
| GO:0035098 | ESC/E(Z) complex | IDA | cellular_component |
| GO:0042054 | Histone methyltransferase activity | IDA | molecular_function |
| GO:0042127 | Regulation of cell proliferation | IEA | biological_process |
| GO:0043406 | Positive regulation of MAP kinase activity | IDA | biological_process |
| GO:0043565 | Sequence-specific DNA binding | IEA | molecular_function |
| GO:0045120 | Pronucleus | IEA | cellular_component |
| GO:0045605 | Negative regulation of epidermal cell differentiation | IEA | biological_process |
| GO:0045814 | Negative regulation of gene expression, epigenetic | IDA | biological_process |
| GO:0045892 | Negative regulation of transcription, DNA-templated | IMP | biological_process |
| GO:0048387 | Negative regulation of retinoic acid receptor signaling pathway | IMP | biological_process |
| GO:0051154 | Negative regulation of striated muscle cell differentiation | IEA | biological_process |
| GO:0070314 | G1 to G0 transition | IEA | biological_process |
| GO:0070734 | Histone H3-K27 methylation | IEA | biological_process |
| GO:0071902 | Positive regulation of protein serine/threonine kinase activity | IDA | biological_process |
| GO:2000134 | Negative regulation of G1/S transition of mitotic cell cycle | IEA | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
| p-value up | p-value down | FDR up | FDR down |
|---|---|---|---|
| 0.9519323886 | 0.0001922001 | 0.9999902473 | 0.0248226415 |
- 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 | -0.4231817183 |
| GSE13712_SHEAR | Up | 0.1256521652 |
| GSE13712_STATIC | Up | 0.0731026663 |
| GSE19018 | Down | -0.9920537525 |
| GSE19899_A1 | Down | -1.4060894978 |
| GSE19899_A2 | Down | -2.9444506593 |
| PubMed_21979375_A1 | Down | -0.7222922335 |
| PubMed_21979375_A2 | Down | -3.3503033167 |
| GSE35957 | Down | -2.8216393897 |
| GSE36640 | Down | -4.3889228292 |
| GSE54402 | Down | -0.0618551471 |
| GSE9593 | Down | -1.8521663914 |
| GSE43922 | Down | -0.7190895817 |
| GSE24585 | Up | 0.3873439178 |
| GSE37065 | Up | 0.0102621576 |
| GSE28863_A1 | Up | 0.0730700605 |
| GSE28863_A2 | Up | 0.6749608476 |
| GSE28863_A3 | Down | -0.5962213700 |
| GSE28863_A4 | Up | 0.0537667696 |
| GSE48662 | Down | -1.4149171365 |
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-214-3p | MIMAT0000271 | MIRT000148 | Luciferase reporter assay//Northern blot | Functional MTI | 19818710 |
| hsa-miR-101-3p | MIMAT0000099 | MIRT000381 | Luciferase reporter assay//Western blot | Functional MTI | 19258506 |
| hsa-miR-101-3p | MIMAT0000099 | MIRT000381 | Luciferase reporter assay//Reporter assay | Functional MTI | 14697198 |
| hsa-miR-101-3p | MIMAT0000099 | MIRT000381 | Luciferase reporter assay//qRT-PCR//Western blot | Functional MTI | 19008416 |
| hsa-miR-101-3p | MIMAT0000099 | MIRT000381 | Luciferase reporter assay | Functional MTI | 19625769 |
| hsa-miR-101-3p | MIMAT0000099 | MIRT000381 | Luciferase reporter assay | Functional MTI | 19043531 |
| hsa-miR-101-3p | MIMAT0000099 | MIRT000381 | qRT-PCR | Functional MTI (Weak) | 20712078 |
| hsa-miR-101-3p | MIMAT0000099 | MIRT000381 | Luciferase reporter assay//qRT-PCR//Western blot | Functional MTI | 20478051 |
| hsa-miR-101-3p | MIMAT0000099 | MIRT000381 | Northern blot | Non-Functional MTI (Weak) | 19818710 |
| hsa-miR-26a-5p | MIMAT0000082 | MIRT001771 | Luciferase reporter assay//Western blot | Functional MTI | 18713946 |
| hsa-miR-26a-5p | MIMAT0000082 | MIRT001771 | Luciferase reporter assay//qRT-PCR//Western blot | Functional MTI | 20478051 |
| hsa-miR-26a-5p | MIMAT0000082 | MIRT001771 | Immunohistochemistry//qRT-PCR//Western blot | Functional MTI | 21199804 |
| hsa-miR-26a-5p | MIMAT0000082 | MIRT001771 | Immunohistochemistry//Luciferase reporter assay//qRT-PCR//Western blot | Functional MTI | 20952513 |
| hsa-miR-26a-5p | MIMAT0000082 | MIRT001771 | Reporter assay | Functional MTI | 18281287 |
| hsa-miR-199a-5p | MIMAT0000231 | MIRT003809 | Luciferase reporter assay//Northern blot | Non-Functional MTI | 19818710 |
| hsa-miR-217 | MIMAT0000274 | MIRT004010 | Luciferase reporter assay//qRT-PCR//Western blot | Non-Functional MTI | 19008416 |
| hsa-miR-124-3p | MIMAT0000422 | MIRT006479 | Immunohistochemistry//Luciferase reporter assay//qRT-PCR//Western blot//Reporter assay;qRT-PCR | Functional MTI | 21672940 |
| hsa-miR-124-3p | MIMAT0000422 | MIRT006479 | Proteomics | Functional MTI (Weak) | 18668037 |
| hsa-miR-98-5p | MIMAT0000096 | MIRT005721 | Northern blot | Non-Functional MTI (Weak) | 19818710 |
| hsa-miR-25-3p | MIMAT0000081 | MIRT006919 | Luciferase reporter assay//qRT-PCR//Western blot | Functional MTI | 22399519 |
| hsa-miR-30d-5p | MIMAT0000245 | MIRT006920 | Luciferase reporter assay//qRT-PCR//Western blot | Functional MTI | 22399519 |
| hsa-miR-138-5p | MIMAT0000430 | MIRT007300 | Luciferase reporter assay//qRT-PCR//Western blot | Functional MTI | 23343715 |
| hsa-miR-138-5p | MIMAT0000430 | MIRT007300 | Reporter assay;Western blot;qRT-PCR;Other | Functional MTI | 21770894 |
| hsa-miR-193b-3p | MIMAT0002819 | MIRT016450 | Microarray | Functional MTI (Weak) | 20304954 |
| hsa-miR-92b-3p | MIMAT0003218 | MIRT040605 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-484 | MIMAT0002174 | MIRT041927 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-320a | MIMAT0000510 | MIRT044834 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-93-5p | MIMAT0000093 | MIRT048778 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-let-7a-5p | MIMAT0000062 | MIRT052566 | CLASH | Functional MTI (Weak) | 23622248 |
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- mirRecord
MicroRNA name | mirBase ID | Target site number | MiRNA mature ID | Test method inter | MiRNA regulation site | Reporter target site | Pubmed ID |
|---|---|---|---|---|---|---|---|
| hsa-miR-26a-5p | MIMAT0000082 | 1 | hsa-miR-26a | 18713946 | |||
| hsa-miR-101-3p | MIMAT0000099 | 1 | hsa-miR-101 | {Immunoblot analysis} | {overexpression by miRNA precursor transfection} | 19008416 | |
| hsa-miR-101-3p | MIMAT0000099 | 2 | hsa-miR-101 | {Immunoblot analysis} | {overexpression by miRNA precursor transfection} | 19008416 | |
| hsa-miR-26a-5p | MIMAT0000082 | 1 | hsa-miR-26a | 18713946 | |||
| hsa-miR-26a-5p | MIMAT0000082 | 1 | hsa-miR-26a | Western blot | {overexpression by mature miRNA transfection} | 20478051 |
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6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 29 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
|---|---|
| 27228653 | Induction of AD in mouse MSC of the C3H10T1/2 cell line was associated with an increase in the expression levels of BMI1, the genes of pRb family (RB, p130) and demethylase UTX, but not methyltransferase EZH2, whose products regulate the methylation levels of H3K27 |
| 27147278 | Prominent examples include aberrations in cytokines and their signaling pathways (such as tumor necrosis factor-alpha, interferon-gamma, SMAD proteins), mutations in genes encoding the RNA splicing machinery (SF3B1, SRSF2, ZRSR2, and U2AF1 genes), mutations in genes disrupting the epigenetic machinery (TET2, DNMT3A, DNMT3B, EZH2, ASXL1) |
| 27129219 | We identified histone methyltransferase EZH2, the catalytic subunit of polycomb repressive complex 2, as a target of Wnt/beta-catenin signaling |
| 27129219 | HBP1-mediated repression of EZH2 through Wnt/beta-catenin signaling decreased the level of trimethylation of histone H3 at lysine 27 of overall and specific histone on the p21 promoter, resulting in p21 transactivation |
| 26579445 | EZH2 is over-expressed in human colon cancer and is closely associated with tumor proliferation, metastasis and poor prognosis |
| 26579445 | Targeting and inhibiting EZH2 may be an effective therapeutic strategy for colon cancer |
| 26579445 | 3-Deazaneplanocin A (DZNep), as an EZH2 inhibitor, can suppress cancer cell growth |
| 26004298 | Enhancer of zeste homolog 2 depletion induces cellular senescence via histone demethylation along the INK4/ARF locus |
| 26004298 | As a member of PcG proteins, enhancer of zeste homolog 2 (EZH2) targets cell cycle regulatory proteins which govern cell cycle progression and cellular senescence |
| 26004298 | In previous work, we reported that EZH2 depletion functionally induced cellular senescence in human gastric cancer cells with mutant p53 |
| 26004298 | However, whether EZH2 expression contributes to the change of key cell cycle regulators and the mechanism involved are still unclear |
| 26004298 | To address this issue, we investigated the effects of EZH2 depletion on alteration of histone methylation pattern |
| 26004298 | In gastric cancer cells, INK4/ARF locus was activated to certain extent in consequence of a decrease of H3K27me3 along it caused by EZH2 silence, which contributed substantially to an increase in the expression of p15(INK4b), p14(ARF) and p16(INK4a) and resulted in cellular senescence ultimately |
| 26004298 | Furthermore, MKN28 cells, which did not express p16(INK4a) and p21(cip), could be induced to senescence via p15(INK4b) activation and suppression of p15(INK4b) reversed senescence progression induced by EZH2 downregulated |
| 26004298 | These data unravel a crucial role of EZH2 in the regulation of INK4/ARF expression and senescence procedure in gastric cancer cells, and show that the cellular senescence could just depend on the activation of p15(INK4b)/Rb pathway, suggesting the cell-type and species specificity involved in the mechanisms of senescence inducement |
| 25772242 | We show that MOZ is required to maintain normal levels of histone 3 lysine 9 (H3K9) and H3K27 acetylation at the transcriptional start sites of at least four genes, Cdc6, Ezh2, E2f2 and Melk, and normal mRNA levels of these genes |
| 25772242 | CDC6, EZH2 and E2F2 are known inhibitors of the INK4A-ARF pathway |
| 25772242 | Using chromatin immunoprecipitation, we show that MOZ occupies the Cdc6, Ezh2 and Melk loci, thereby providing a direct link between MOZ, H3K9 and H3K27 acetylation, and normal transcriptional levels at these loci |
| 25289642 | Special emphasis on expression of a polycomb group protein EZH2 and a senescent marker p16INK4a in bile ductular tumors and lesions |
| 25289642 | Given overexpression of a polycomb group protein EZH2 in intrahepatic cholangiocarcinoma and high expression of senescence-associated p16INK4a in ductular reactions, we plan to apply immunostaining for EZH2 and p16INK4a for differential diagnosis of these bile ductular tumors/lesions |
| 25289642 | The expression of EZH2 was seen in all cases of cholangiolocellular carcinomas, while it was not observed in bile duct adenomas or ductular reactions |
| 25289642 | A borderline between cholangiolocellular carcinoma and the surrounding ductular reaction was clearly highlighted by the reverse expression pattern of EZH2 and p16INK4a |
| 25289642 | In conclusion, immunostaining for EZH2 and p16INK4a may be useful for differential diagnosis for bile ductular tumors/lesions |
| 25264199 | Here, using a comprehensive collection of cancer microarray data, we found FOXA1 is down-regulated in many cancers compared to their normal counterparts and the positive correlation between FOXA1 and CDKN2A could be observed in prostate and breast cancers with lower EZH2 (epigenetic repressor for CDKN2A) expression |
| 25264199 | Experimentally, epistasis analysis in prostate and breast cancer cells indicated that higher expression of FOXA1 opposes EZH2-mediated CDKN2A repression, as further depletion of FOXA1 reverts the de-silencing of CDKN2A caused by EZH2 inhibition |
| 25264199 | A further oncogenic transformation assay suggested that overexpression of EZH2 is insufficient to block RAS-induced CDKN2A activation and loss of FOXA1 is mandatory to potentiate EZH2-mediated CDKN2A silencing and to bypass the senescence barrier |
| 25264199 | These data support that positive regulation of CDKN2A by FOXA1 counteracts its tumorigenic repression of by EZH2 in cancers |
| 25255445 | Regulation of p53 and Rb links the alternative NF-kappaB pathway to EZH2 expression and cell senescence |
| 25255445 | These combine to regulate the activity of the retinoblastoma protein, Rb, leading to induction of polycomb protein EZH2 expression |
| 25255445 | Moreover, our ChIP analysis demonstrates that EZH2 is also a direct NF-kappaB target gene |
| 25255445 | Microarray analysis revealed that in fibroblasts, EZH2 antagonizes a subset of p53 target genes previously associated with the senescent cell phenotype, including DEK and RacGAP1 |
| 25255445 | Importantly, we find that activation of NF-kappaB also induces EZH2 expression in CD40L stimulated cells from Chronic Lymphocytic Leukemia patients |
| 24738879 | OBJECTIVES: Enhancer of zeste homologue 2 (EZH2) is crucially involved in epigenetic silencing by acting as a histone methyltransferase |
| 24738879 | Although EZH2 is overexpressed in many cancers and is involved in malignant cell proliferation and invasion, the role of EZH2 in senescence induced by DNA damage has up to now remained largely unknown |
| 24738879 | In this study, we sought to explore the outcome of EZH2 depletion along with exposure of doxorubicin (DOX), and related mechanisms, in gastric cancer cells |
| 24738879 | EZH2 was downregulated by transfection with siRNA or treated with (-)-epigallocatechin-3-gallate, a targeted inhibitor |
| 24738879 | To investigate effects of EZH2 depletion on the cell cycle, apoptosis and proliferation, flow cytometry and MTT analysis were employed |
| 24738879 | RESULTS: We found that cell proliferative arrest caused by DOX could be promoted by EZH2 depletion |
| 24738879 | Mechanistically, EZH2 depletion not only worked in coordination with DNA damage during the progression of cell senescence but also promoted apoptosis in p53 mutant cells |
| 24738879 | CONCLUSIONS: These data help unravel a crucial role for EZH2 in senescence and apoptosis in gastric cancer cells and that p53 genomic status was associated with different cell responses to EZH2 silencing |
| 24588771 | Enhancer of zeste homolog 2 (EZH2) as a member of polycomb group proteins and its targets include cell cycle regulatory proteins, which govern cell cycle progression and cellular senescence |
| 24588771 | In this study, we report that EZH2 depletion promotes the senescent state in human gastric cancer cells SGC-7901 |
| 24588771 | We found that EZH2 functionally suppressed the senescent state in human gastric cancer cells SGC-7901 |
| 24588771 | EZH2 depletion inhibited cell proliferation, arrested cellular cycle, restored features of a cellular senescence phenotype, and promoted doxorubicin-induced senescence |
| 24588771 | To prove that EZH2 expression contributes substantially to the change of key cell cycle regulators, we showed that p21 and p16 were activated to a certain extent upon EZH2 depletion and activation of p21 was in a p53-independent manner |
| 24588771 | Taken together, our data suggest that EZH2 depletion promotes the progression of senescence by mediating the activation of tumor suppressor genes p21 and p16, and could serve as a potential epigenetic target for gastric cancer therapy |
| 24487593 | Immunostaining for polycomb group protein EZH2 and senescent marker p16INK4a may be useful to differentiate cholangiolocellular carcinoma from ductular reaction and bile duct adenoma |
| 24487593 | We have previously reported that cholangiolocellular carcinoma showed overexpression of a polycomb group protein EZH2, which participates in bypass/escape from cellular senescence during carcinogenesis |
| 24487593 | In this study, we examined whether immunostaining for EZH2 and p16(INK4a) is useful for differential diagnosis among cholangiolocellular carcinoma, bile duct adenoma, and ductular reactions |
| 24487593 | The expressions of EZH2 and p16(INK4a) were examined immunohistochemically |
| 24487593 | The expression of EZH2 was seen in all cases of cholangiolocellular carcinomas, but it was not observed in bile duct adenomas and ductular reactions, which were seen around carcinomas in 80% of cases |
| 24487593 | The borderline between the component of cholangiolocellular carcinoma and the surrounding ductular reaction was clearly highlighted by the reverse expression pattern of EZH2 and p16(INK4a) in 69% of cases |
| 24487593 | In conclusion, immunostaining for EZH2 and p16(INK4a) may be useful for differential diagnosis among cholangiolocellular carcinomas, bile duct adenomas, and ductular reactions |
| 24406044 | MiR-138 induces renal carcinoma cell senescence by targeting EZH2 and is downregulated in human clear cell renal cell carcinoma |
| 24406044 | Additionally, knockdown of EZH2 by its siRNA was performed |
| 24406044 | Transfection of miR-138 mimic induced SN-12 cell senescence, decreased the protein expression of EZH2, and increased the protein expression of P16 |
| 24406044 | Furthermore, miR-138 decreased the 3'UTR luciferase activity of EZH2 |
| 24406044 | The knockdown of EZH2 by siRNA induced SN-12 cell senescence, decreased the protein expression level of EZH2, and increased the protein expression of P16 |
| 24406044 | MiR-138 is a tumor-suppressor miRNA in ccRCC that induces SN-12 cell senescence by downregulating EZH2 expression and upregulating P16 expression |
| 24217920 | We show that SA-miRNAs-26b, 181a, 210 and 424 function in concert to directly repress expression of Polycomb group (PcG) proteins CBX7, embryonic ectoderm development (EED), enhancer of zeste homologue 2 (EZH2) and suppressor of zeste 12 homologue (Suz12), thereby activating p16 |
| 23826727 | The activation of E2F transcriptional factors leads to methylation of p16(ink4a) promoter, an event that is mediated by the upregulation of polycomb protein, Ezh2 |
| 23788032 | It is known that the histone methyltransferase enhancer of zeste homolog 2 (EZH2) and embryonic ectoderm development (EED) are direct targets of miR-101 |
| 23788032 | The epigenetic regulation of H3K27me3 on CPEB1 promoter is mediated by EZH2 and EED |
| 23788032 | EZH2 has a role in the regulation of H3K4me2 |
| 23557329 | Subsequent analysis was focused on miR-101 and its putative target gene Ezh2 |
| 23557329 | We confirmed that Ezh2 is regulated by miR-101 in human fibroblasts, and found that both overexpression of miR-101 and downregulation of Ezh2 independently induce senescence in the absence of UVB irradiation |
| 23557329 | In addition, miR-101 and Ezh2 were identified as key players in UVB-induced senescence of HDF |
| 21757686 | Lysine-specific demethylase 2B (KDM2B)-let-7-enhancer of zester homolog 2 (EZH2) pathway regulates cell cycle progression and senescence in primary cells |
| 21757686 | Here, we show that KDM2B is a conserved regulator of lifespan in multiple primary cell types and defines a program in which this chromatin-modifying enzyme counteracts the senescence-associated down-regulation of the EZH2 histone methyltransferase |
| 21757686 | Forced expression of KDM2B promotes immortalization by silencing these miRNAs through locus-specific histone H3 K36me2 demethylation, leading to EZH2 up-regulation |
| 21757686 | Overexpression of let-7b down-regulates EZH2, induces premature senescence, and counteracts immortalization of MEFs driven by KDM2B |
| 21572997 | DNA methyltransferase controls stem cell aging by regulating BMI1 and EZH2 through microRNAs |
| 21572997 | Enrichment of EZH2, the key factor that methylates histone H3 lysine 9 and 27 residues, was decreased on the p16(INK4A) and p21(CIP1/WAF1) promoter regions |
| 21559395 | Consistent with this hypothesis, EWS-FLI1 induced hNCSC genes as well as the polycomb proteins BMI-1 and EZH2 in hNC-MSC |
| 21383005 | Polycomb group (PcG) proteins such as Enhancer of zeste homolog 2 (EZH2) are epigenetic transcriptional repressors that function through recognition and modification of histone methylation and chromatin structure |
| 21383005 | In this study, we report that EZH2, which we find absent in melanocytic nevi but expressed in many or most metastatic melanoma cells, functionally suppresses the senescent state in human melanoma cells |
| 21383005 | EZH2 depletion in melanoma cells inhibits cell proliferation, restores features of a cellular senescence phenotype, and inhibits growth of melanoma xenografts in vivo |
| 21383005 | EZH2 depletion removes histone deacetylase 1 (HDAC1) from the CDKN1A transcriptional start site and downstream region, enhancing histone 3 acetylation globally and at CDKN1A |
| 21383005 | Depletion of EZH2 synergistically activates p21/CDKN1A expression in combination with the HDAC inhibitor trichostatin A |
| 21383005 | Since melanomas often retain wild-type p53 function activating p21, our findings describe a novel mechanism whereby EZH2 activation during tumor progression represses p21, leading to suppression of cellular senescence and enhanced tumorigenicity |
| 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 |
| 19954516 | During progenitor cell differentiation and ageing, PcG silencer EZH2 attenuates, causing loss of PRC binding and transcriptional activation of INK4b and INK4a |
| 19954516 | Down regulation of EZH2 causes release of the approximately 35 kb repressive chromatin loop and induction of both INK4a and INK4b, whereas ARF expression remains unaltered |
| 19954516 | Developmentally regulated EZH2 levels are one of the factors that can determine the higher order chromatin structure and expression pattern of the INK4b-ARF-INK4a locus, coupling human progenitor cell differentiation to proliferation control |
| 19564843 | In contrast, EZH2, a polycomb group protein, was overexpressed in intraepithelial neoplasm and carcinoma in gallbladders with cholecystolithiasis |
| 19564843 | Conversely, enforced overexpression of EZH2 in senescent HGECs reduced p16(INK4A) expression |
| 19564843 | A knockdown of EZH2 in cultured TGBC2TKB cells increased p16(INK4a) expression |
| 19564843 | EZH2 may be responsible for the escape from cellular senescence followed by malignant transformation in the gallbladder of PBM |
| 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 |
| 17344414 | Significantly, EZH2 is down-regulated in stressed and senescing populations of cells, coinciding with decreased levels of associated H3K27me3, displacement of BMI1, and activation of transcription |
| 17332078 | Epigenetic control of hematopoietic stem cell aging the case of Ezh2 |
| 17332078 | We provide evidence for the involvement of one of these Polycomb group genes, Ezh2, in aging of the hematopoietic stem cell system |
| 16293602 | The Polycomb group gene Ezh2 prevents hematopoietic stem cell exhaustion |
| 16293602 | In proliferating and senescent MEFs one of the most differentially expressed transcripts was Enhancer of zeste homolog 2 (Ezh2), a Polycomb group protein (PcG) involved in histone methylation and deacetylation |
| 16293602 | Retroviral overexpression of Ezh2 in MEFs resulted in bypassing of the senescence program |
| 16293602 | More importantly, whereas normal HSCs were rapidly exhausted after serial transplantations, overexpression of Ezh2 completely conserved long-term repopulating potential |
| 16293602 | In a "genetic genomics" screen, we identified novel putative Ezh2 target or partner stem cell genes that are associated with chromatin modification |
| 15208672 | Activated p53 suppresses the histone methyltransferase EZH2 gene |
| 15208672 | The histone methyltransferase (HMTase), EZH2, was specifically downregulated in senescent cells |
| 15208672 | Activated p53 suppressed EZH2 gene expression through repression of the EZH2 gene promoter |
| 15208672 | Furthermore, the repression of EZH2 promoter by p53 is dependent on p53 transcriptional target p21(Waf1) inactivating RB/E2F pathways |
| 15208672 | In addition, the knockdown of EZH2 expression retards cell proliferation and induces G2/M arrest |
| 15208672 | We suggest that the p53-dependent suppression of EZH2 expression is a novel pathway that contributes to p53-mediated G2/M arrest |
| 15208672 | EZH2 associated complex possesses HMTase activity and is involved in epigenetic regulation |
| 15208672 | Activated p53 suppresses EZH2 expression, suggesting a further role for p53 in epigenetic regulation and in the maintenance of genetic stability |
| 15208672 | Suppression of EZH2 expression in tumors by p53 may lead to novel approaches to control cancer progression |
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