About Enhancer
| Enhancer ID: | E_02_0498 |
| Species: | human |
| Position : | chr14:100235442-100237442   |
| Biosample name: | |
| Experiment class : | High+Lowthroughput |
| Enhancer type: | Enhancer |
| Disease: | Chicken pox |
| Pubmed ID: | 30076309 |
| Enhancer experiment: | Chip PCR, RNA SEQ, ATAC SEQ, statistical analysis, Western blot |
| Enhancer experiment description: | The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals. Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33. |
About Target gene
| Target gene : | YY1(DELTA,GADEVS,INO80S,NF-E1,UCRBP,YIN-YANG-1),DUSP6,PTPN22,DUSP5,PTEN |
| Strong evidence: | qRT-PCR,qPCR,ChIP,3C |
| Less strong evidence: | RNA-Seq |
| Target gene experiment description: | The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals. Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.;The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals. Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.;The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals. Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.;The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals. Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.;The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals. Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33. |
About TF
| TF name : | -- |
| TF experiment: | ChIP-PCR,RNA-seq,ATAC-seq,????,western blot |
| TF experiment description: | The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals. Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.;The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals. Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.;The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals. Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.;The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals. Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.;The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals. Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33. |
About Function
| Enhancer function : | The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals. Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33. |
| Enhancer function experiment: | Immunohistochemical staining |
| Enhancer function experiment description: |
The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals. Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33. |
About SNP
| SNP ID: | -- |
Upstream Pathway Annotation of TF
| GeneName | Pathway Name | Source | Gene Number |
|---|
Enhancer associated network
The number on yellow line represents the distance between enhancer and
target gene