Enhancer ID: | E_01_251 | |
Enhancer symbol: | NGB Enhancer | |
Species: | Human | |
Position : | chr14:77635927-77639784 |
|
Biosample name: | SH-SY5Y | |
Experiment class : | low throughput |
Enhancer type: | Enhancer | |
Disease: | Alzheimer's Disease | |
DO: | DOID:10652 | |
Mesh: | D000544 | |
Distance from TSS: | >2KB | |
Pubmed ID: | 27651453 |
Enhancer experiment: | 3C,Luciferase Reporter Assay,ChIP,CRISPR/Cas9 | |
Enhancer experiment description: | By chromosome conformation capture we identified two novel DREs located −70 kb upstream and +100 kb downstream from the NGB gene. ENCODE database showed the presence of DNaseI hypersensitive and transcription factors binding sites in these regions. Further analyses using luciferase reporters and chromatin immunoprecipitation suggested that the −70 kb region upstream of the NGB gene contained a neuronal-specific enhancer and GATA transcription factor binding sites. To further illustrate the importance of Element I in inducing expression of the NGB gene, Element I was deleted from SH-SY5Y cells by the CRISPR/Cas9 system. We found that deletion of Element I signiicantly decreased NGB expression levels to 13–25%of those observed in control SH-SY5Y cells (Figure 4C). |
Target gene : | NGB(NGB) | |
Strong evidence: | 3C | |
Less strong evidence: | Luciferase Reporter Assay,ChIP | |
Target gene experiment description: | By chromosome conformation capture we identified two novel DREs located −70 kb upstream and +100 kb downstream from the NGB gene. ENCODE database showed the presence of DNaseI hypersensitive and transcription factors binding sites in these regions. Further analyses using luciferase reporters and chromatin immunoprecipitation suggested that the −70 kb region upstream of the NGB gene contained a neuronal-specific enhancer and GATA transcription factor binding sites. |
TF name : | GATA2(DCML,IMD21,MONOMAC,NFE1B) | |
TF experiment: | Luciferase Reporter Assay,ChIP,shRNA | |
TF experiment description: | Further analyses using luciferase reporters and chromatin immunoprecipitation suggested that the −70 kb region upstream of the NGB gene contained a neuronal- specific enhancer and GATA transcription factor binding sites. Knockdown of GATA-2 caused NGB expression to drop dramatically, indicating GATA-2 as an essential transcription factor for the activation of NGB expression. |
Enhancer function : | Deletion of element I reduces NGB gene expression |
Enhancer function experiment: | Luciferase Reporter Assay,CRISPR/Cas9 |
Enhancer function experiment description: |
The regulatory roles of Element I and GATA-2 were demonstrated by the luciferase reporter and knockdown experiments respectively. To further illustrate the importance of Element I in inducing expression of the NGB gene, Element I was deleted from SH-SY5Y cells by the CRISPR/Cas9 system. We found that deletion of Element I signiicantly decreased NGB expression levels to 13–25%of those observed in control SH-SY5Y cells (Figure 4C). |
SNP ID: | -- | |
SNP position: | -- |
SNP experiment: | -- |
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