About Enhancer
| Enhancer ID: | E_01_0645 |
| Species: | human |
| Position : | chr2:226728494-226730494   |
| Biosample name: | |
| Experiment class : | High+Lowthroughput |
| Enhancer type: | Enhancer |
| Disease: | Type 2 diabetes mellitus |
| Pubmed ID: | 30826407 |
| Enhancer experiment: | Nuclear magnetic resonance (NMR) spectroscopy analysis ?RNA extraction and real-time PCR ?Western blot analysis ?Histopathological analysis ,Analysis of glycated hemoglobin and ?-cell function |
| Enhancer experiment description: | Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance. The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). |
About Target gene
| Target gene : | IRS1(HIRS-1) |
| Strong evidence: | qRT-PCR,qPCR,ChIP,3C |
| Less strong evidence: | RNA-Seq |
| Target gene experiment description: | Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance. The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). |
About TF
| TF name : | -- |
| TF experiment: | Nuclear magnetic resonance (NMR) spectroscopy analysis ?RNA extraction and real-time PCR ?Western blot analysis ?Histopathological analysis ,Analysis of glycated hemoglobin and ?-cell function |
| TF experiment description: | Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance. The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). |
About Function
| Enhancer function : | Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance. The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). |
| Enhancer function experiment: | Immunohistochemical staining |
| Enhancer function experiment description: |
Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance. The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). |
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