About Enhancer
| Enhancer ID: | E_01_0405 |
| Species: | human |
| Position : | chrX:67541571-67543571   |
| Biosample name: | |
| Experiment class : | High+Lowthroughput |
| Enhancer type: | Enhancer |
| Disease: | Prostatic cancer |
| Pubmed ID: | 29909987 |
| Enhancer experiment: | PCR,CRISPR/Cas9,Proliferation Assays,Competition Experiments,Quantitative RT-PCR,Immunoblotting,Cloning,Chromosome Conformation Capture(3C),Crystal Violet Proliferation Assays,ChIP-seq,ChIP,ChIP-qPCR,Whole-Genome Bisulfite Sequencing analysis(WGBS), |
| Enhancer experiment description: | Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers. |
About Target gene
| Target gene : | EIF4A3,SF3B3,RPL23 |
| Strong evidence: | qRT-PCR,qPCR,ChIP,3C |
| Less strong evidence: | RNA-Seq |
| Target gene experiment description: | Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers.;Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers.;Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers.;Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers. |
About TF
| TF name : | AR(AIS8,DHTR,HUMARA,HYSP1,KD,NR3C4,SBMA,SMAX1,TFM,AR) |
| TF experiment: | PCR,CRISPR/Cas9,Proliferation Assays,Competition Experiments,Quantitative RT-PCR,Immunoblotting,Cloning,Chromosome Conformation Capture(3C),Crystal Violet Proliferation Assays,ChIP-seq,ChIP,ChIP-qPCR,Whole-Genome Bisulfite Sequencing analysis(WGBS), |
| TF experiment description: | Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers.;Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers.;Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers.;Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers. |
About Function
| Enhancer function : | Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers. |
| Enhancer function experiment: | Immunohistochemical staining |
| Enhancer function experiment description: |
Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers. |
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