Enhancer ID: | E_02_0492 |
Species: | human |
Position : | chr14:100776351-100778351 |
Biosample name: | |
Experiment class : | High+Lowthroughput |
Enhancer type: | Enhancer |
Disease: | Type 2 diabetes mellitus (t2dm) |
Pubmed ID: | 30084829 |
Enhancer experiment: | ChIP-PCR,4C-Seq,RT-PCR |
Enhancer experiment description: | In this study, using targeted epigenetic modifiers, we prove that increased methylation at the promoter of Meg3 in mouse ?TC6 ?-cells results in decreased transcription of the maternal transcripts associated with this locus. Using circular chromosome conformation capture followed by high-throughput sequencing, we demonstrate that the promoter of MEG3 physically interacts with this novel enhancer and other putative regulatory elements in this imprinted region in human islets. Remarkably, this enhancer is bound in an allele-specific manner by the transcription factors FOXA2, PDX1, and NKX2.2. |
Target gene : | MEG3(2900016C05Rik,3110050O07Rik,6330408G06Rik,AI425946,AW108224,D12Bwg1266e,Gtl2,R74756,R75394),FOXA2,PDX1(IDX-1,IPF-1,Ipf1,Mody4,STF-1,pdx-1) |
Strong evidence: | qRT-PCR,qPCR,ChIP,3C |
Less strong evidence: | RNA-Seq |
Target gene experiment description: | In this study, using targeted epigenetic modifiers, we prove that increased methylation at the promoter of Meg3 in mouse ?TC6 ?-cells results in decreased transcription of the maternal transcripts associated with this locus. Using circular chromosome conformation capture followed by high-throughput sequencing, we demonstrate that the promoter of MEG3 physically interacts with this novel enhancer and other putative regulatory elements in this imprinted region in human islets. Remarkably, this enhancer is bound in an allele-specific manner by the transcription factors FOXA2, PDX1, and NKX2.2. ;In this study, using targeted epigenetic modifiers, we prove that increased methylation at the promoter of Meg3 in mouse ?TC6 ?-cells results in decreased transcription of the maternal transcripts associated with this locus. Using circular chromosome conformation capture followed by high-throughput sequencing, we demonstrate that the promoter of MEG3 physically interacts with this novel enhancer and other putative regulatory elements in this imprinted region in human islets. Remarkably, this enhancer is bound in an allele-specific manner by the transcription factors FOXA2, PDX1, and NKX2.2. ;In this study, using targeted epigenetic modifiers, we prove that increased methylation at the promoter of Meg3 in mouse ?TC6 ?-cells results in decreased transcription of the maternal transcripts associated with this locus. Using circular chromosome conformation capture followed by high-throughput sequencing, we demonstrate that the promoter of MEG3 physically interacts with this novel enhancer and other putative regulatory elements in this imprinted region in human islets. Remarkably, this enhancer is bound in an allele-specific manner by the transcription factors FOXA2, PDX1, and NKX2.2. |
TF name : | -- |
TF experiment: | ChIP-PCR,4C-Seq,RT-PCR |
TF experiment description: | In this study, using targeted epigenetic modifiers, we prove that increased methylation at the promoter of Meg3 in mouse ?TC6 ?-cells results in decreased transcription of the maternal transcripts associated with this locus. Using circular chromosome conformation capture followed by high-throughput sequencing, we demonstrate that the promoter of MEG3 physically interacts with this novel enhancer and other putative regulatory elements in this imprinted region in human islets. Remarkably, this enhancer is bound in an allele-specific manner by the transcription factors FOXA2, PDX1, and NKX2.2. ;In this study, using targeted epigenetic modifiers, we prove that increased methylation at the promoter of Meg3 in mouse ?TC6 ?-cells results in decreased transcription of the maternal transcripts associated with this locus. Using circular chromosome conformation capture followed by high-throughput sequencing, we demonstrate that the promoter of MEG3 physically interacts with this novel enhancer and other putative regulatory elements in this imprinted region in human islets. Remarkably, this enhancer is bound in an allele-specific manner by the transcription factors FOXA2, PDX1, and NKX2.2. ;In this study, using targeted epigenetic modifiers, we prove that increased methylation at the promoter of Meg3 in mouse ?TC6 ?-cells results in decreased transcription of the maternal transcripts associated with this locus. Using circular chromosome conformation capture followed by high-throughput sequencing, we demonstrate that the promoter of MEG3 physically interacts with this novel enhancer and other putative regulatory elements in this imprinted region in human islets. Remarkably, this enhancer is bound in an allele-specific manner by the transcription factors FOXA2, PDX1, and NKX2.2. |
Enhancer function : | In this study, using targeted epigenetic modifiers, we prove that increased methylation at the promoter of Meg3 in mouse ?TC6 ?-cells results in decreased transcription of the maternal transcripts associated with this locus. Using circular chromosome conformation capture followed by high-throughput sequencing, we demonstrate that the promoter of MEG3 physically interacts with this novel enhancer and other putative regulatory elements in this imprinted region in human islets. Remarkably, this enhancer is bound in an allele-specific manner by the transcription factors FOXA2, PDX1, and NKX2.2. |
Enhancer function experiment: | Immunohistochemical staining |
Enhancer function experiment description: |
In this study, using targeted epigenetic modifiers, we prove that increased methylation at the promoter of Meg3 in mouse ?TC6 ?-cells results in decreased transcription of the maternal transcripts associated with this locus. Using circular chromosome conformation capture followed by high-throughput sequencing, we demonstrate that the promoter of MEG3 physically interacts with this novel enhancer and other putative regulatory elements in this imprinted region in human islets. Remarkably, this enhancer is bound in an allele-specific manner by the transcription factors FOXA2, PDX1, and NKX2.2. |
SNP ID: | rs3783355 |
GeneName | Pathway Name | Source | Gene Number |
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