About Enhancer
| Enhancer ID: | E_01_0751 |
| Species: | human |
| Position : | chr19:10130546-10132546   |
| Biosample name: | |
| Experiment class : | High+Lowthroughput |
| Enhancer type: | Enhancer |
| Disease: | Hepatocellular carcinoma (hcc), cirrhosis, hepatitis b |
| Pubmed ID: | 30136421 |
| Enhancer experiment: | qRT-PCR ,ChIP-seq,RNA-seq |
| Enhancer experiment description: | While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7). |
About Target gene
| Target gene : | TET3,TET2(Ayu17-449,E130014J05Rik,mKIAA1546) |
| Strong evidence: | qRT-PCR,qPCR,ChIP,3C |
| Less strong evidence: | RNA-Seq |
| Target gene experiment description: | While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).;While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).;While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).;While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).;While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7). |
About TF
| TF name : | DNMT1(ADCADN,AIM,CXXC9,DNMT,HSN1E,MCMT,m.HsaI)DNMT3ATET1 |
| TF experiment: | qRT-PCR ,ChIP-seq,RNA-seq |
| TF experiment description: | While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).;While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).;While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).;While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).;While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7). |
About Function
| Enhancer function : | While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7). |
| Enhancer function experiment: | Immunohistochemical staining |
| Enhancer function experiment description: |
While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7). |
About SNP
| SNP ID: | -- |
Upstream Pathway Annotation of TF
Enhancer associated network
The number on yellow line represents the distance between enhancer and
target gene