About Enhancer
| Enhancer ID: | E_02_0274 |
| Species: | human |
| Position : | chr2:216669369-216671369   |
| Biosample name: | |
| Experiment class : | High+Lowthroughput |
| Enhancer type: | Enhancer |
| Disease: | Dopaminergic neuron apoptosis |
| Pubmed ID: | 29939784 |
| Enhancer experiment: | Luciferase Reporter assay,Western blot,Annexin V apoptosis staining,shRNA and stereotaxic injection,siRNA and transient transfection,TUNEL staining,Electron microscopy,Immunofluorescence labeling, |
| Enhancer experiment description: | We found that, at relatively high doses, Meth exposure increased C/EBP? protein expression, which was accompanied by increased neuronal apoptosis and autophagy; triggered the IGFBP5-mediated, p53-up-regulated modulator of apoptosis (PUMA)-related mitochondrial apoptotic signaling pathway; and stimulated the Trib3-mediated ER stress signaling pathway through the Akt-mTOR signaling axis. We also found that autophagy is an early response to Meth-induced stress upstream of apoptosis and plays a detrimental role in Meth-induced neuronal cell death. These results suggest that Meth exposure induces C/EBP? expression, which plays an essential role in the neuronal apoptosis and autophagy induced by relatively high doses of Meth; however, relatively low concentrations of Meth did not change the expression of C/EBP? in vitro. Further studies are needed to elucidate the role of C/EBP? in low-dose Meth-induced neurotoxicity. |
About Target gene
| Target gene : | IGFBP5(CC-CKR-4,CD194,CKR4,CMKBR4,ChemR13,HGCN:14099,K5-5),Trib3 |
| Strong evidence: | qRT-PCR,qPCR,ChIP,3C |
| Less strong evidence: | RNA-Seq |
| Target gene experiment description: | We found that, at relatively high doses, Meth exposure increased C/EBP? protein expression, which was accompanied by increased neuronal apoptosis and autophagy; triggered the IGFBP5-mediated, p53-up-regulated modulator of apoptosis (PUMA)-related mitochondrial apoptotic signaling pathway; and stimulated the Trib3-mediated ER stress signaling pathway through the Akt-mTOR signaling axis. We also found that autophagy is an early response to Meth-induced stress upstream of apoptosis and plays a detrimental role in Meth-induced neuronal cell death. These results suggest that Meth exposure induces C/EBP? expression, which plays an essential role in the neuronal apoptosis and autophagy induced by relatively high doses of Meth; however, relatively low concentrations of Meth did not change the expression of C/EBP? in vitro. Further studies are needed to elucidate the role of C/EBP? in low-dose Meth-induced neurotoxicity.;We found that, at relatively high doses, Meth exposure increased C/EBP? protein expression, which was accompanied by increased neuronal apoptosis and autophagy; triggered the IGFBP5-mediated, p53-up-regulated modulator of apoptosis (PUMA)-related mitochondrial apoptotic signaling pathway; and stimulated the Trib3-mediated ER stress signaling pathway through the Akt-mTOR signaling axis. We also found that autophagy is an early response to Meth-induced stress upstream of apoptosis and plays a detrimental role in Meth-induced neuronal cell death. These results suggest that Meth exposure induces C/EBP? expression, which plays an essential role in the neuronal apoptosis and autophagy induced by relatively high doses of Meth; however, relatively low concentrations of Meth did not change the expression of C/EBP? in vitro. Further studies are needed to elucidate the role of C/EBP? in low-dose Meth-induced neurotoxicity. |
About TF
| TF name : | -- |
| TF experiment: | Luciferase Reporter assay,Western blot,Annexin V apoptosis staining,shRNA and stereotaxic injection,siRNA and transient transfection,TUNEL staining,Electron microscopy,Immunofluorescence labeling, |
| TF experiment description: | We found that, at relatively high doses, Meth exposure increased C/EBP? protein expression, which was accompanied by increased neuronal apoptosis and autophagy; triggered the IGFBP5-mediated, p53-up-regulated modulator of apoptosis (PUMA)-related mitochondrial apoptotic signaling pathway; and stimulated the Trib3-mediated ER stress signaling pathway through the Akt-mTOR signaling axis. We also found that autophagy is an early response to Meth-induced stress upstream of apoptosis and plays a detrimental role in Meth-induced neuronal cell death. These results suggest that Meth exposure induces C/EBP? expression, which plays an essential role in the neuronal apoptosis and autophagy induced by relatively high doses of Meth; however, relatively low concentrations of Meth did not change the expression of C/EBP? in vitro. Further studies are needed to elucidate the role of C/EBP? in low-dose Meth-induced neurotoxicity.;We found that, at relatively high doses, Meth exposure increased C/EBP? protein expression, which was accompanied by increased neuronal apoptosis and autophagy; triggered the IGFBP5-mediated, p53-up-regulated modulator of apoptosis (PUMA)-related mitochondrial apoptotic signaling pathway; and stimulated the Trib3-mediated ER stress signaling pathway through the Akt-mTOR signaling axis. We also found that autophagy is an early response to Meth-induced stress upstream of apoptosis and plays a detrimental role in Meth-induced neuronal cell death. These results suggest that Meth exposure induces C/EBP? expression, which plays an essential role in the neuronal apoptosis and autophagy induced by relatively high doses of Meth; however, relatively low concentrations of Meth did not change the expression of C/EBP? in vitro. Further studies are needed to elucidate the role of C/EBP? in low-dose Meth-induced neurotoxicity. |
About Function
| Enhancer function : | We found that, at relatively high doses, Meth exposure increased C/EBP? protein expression, which was accompanied by increased neuronal apoptosis and autophagy; triggered the IGFBP5-mediated, p53-up-regulated modulator of apoptosis (PUMA)-related mitochondrial apoptotic signaling pathway; and stimulated the Trib3-mediated ER stress signaling pathway through the Akt-mTOR signaling axis. We also found that autophagy is an early response to Meth-induced stress upstream of apoptosis and plays a detrimental role in Meth-induced neuronal cell death. These results suggest that Meth exposure induces C/EBP? expression, which plays an essential role in the neuronal apoptosis and autophagy induced by relatively high doses of Meth; however, relatively low concentrations of Meth did not change the expression of C/EBP? in vitro. Further studies are needed to elucidate the role of C/EBP? in low-dose Meth-induced neurotoxicity. |
| Enhancer function experiment: | Immunohistochemical staining |
| Enhancer function experiment description: |
We found that, at relatively high doses, Meth exposure increased C/EBP? protein expression, which was accompanied by increased neuronal apoptosis and autophagy; triggered the IGFBP5-mediated, p53-up-regulated modulator of apoptosis (PUMA)-related mitochondrial apoptotic signaling pathway; and stimulated the Trib3-mediated ER stress signaling pathway through the Akt-mTOR signaling axis. We also found that autophagy is an early response to Meth-induced stress upstream of apoptosis and plays a detrimental role in Meth-induced neuronal cell death. These results suggest that Meth exposure induces C/EBP? expression, which plays an essential role in the neuronal apoptosis and autophagy induced by relatively high doses of Meth; however, relatively low concentrations of Meth did not change the expression of C/EBP? in vitro. Further studies are needed to elucidate the role of C/EBP? in low-dose Meth-induced neurotoxicity. |
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