About Enhancer
| Enhancer ID: | E_01_0495 |
| Species: | human |
| Position : | chr17:44900352-44902352   |
| Biosample name: | |
| Experiment class : | High+Lowthroughput |
| Enhancer type: | Enhancer |
| Disease: | Parkinson's disease (pd) |
| Pubmed ID: | 29749529 |
| Enhancer experiment: | Immunofluorescence,Immunoassay,Western blot, CHOP Knockdown,transfection,Immunostaining,flow cytometry,RNA-seq,siRNA, |
| Enhancer experiment description: | In addition, Golgi fragmentation was observed in the process. On the other hand, it was also demonstrated, in a primary neuronal?astroglial co?culture system, that the overexpression of ??syn significantly decreased the levels of glia?derived neurotrophic factor (GDNF) and partly inhibited neurite outgrowth. Although direct evidence is currently lacking, it was proposed that dysfunction of the ER?Golgi compartment in astrocytes overexpressing ??syn may lead to a decline of GDNF levels, which in turn would suppress neurite outgrowth. Taken together, the results of the present study offer further insights into the pathogenesis of PD from the perspective of astrocytes, which may provide novel strategies for the diagnosis and treatment of PD in the future. |
About Target gene
| Target gene : | MAP2 |
| Strong evidence: | qRT-PCR,qPCR,ChIP,3C |
| Less strong evidence: | RNA-Seq |
| Target gene experiment description: | In addition, Golgi fragmentation was observed in the process. On the other hand, it was also demonstrated, in a primary neuronal?astroglial co?culture system, that the overexpression of ??syn significantly decreased the levels of glia?derived neurotrophic factor (GDNF) and partly inhibited neurite outgrowth. Although direct evidence is currently lacking, it was proposed that dysfunction of the ER?Golgi compartment in astrocytes overexpressing ??syn may lead to a decline of GDNF levels, which in turn would suppress neurite outgrowth. Taken together, the results of the present study offer further insights into the pathogenesis of PD from the perspective of astrocytes, which may provide novel strategies for the diagnosis and treatment of PD in the future.;In addition, Golgi fragmentation was observed in the process. On the other hand, it was also demonstrated, in a primary neuronal?astroglial co?culture system, that the overexpression of ??syn significantly decreased the levels of glia?derived neurotrophic factor (GDNF) and partly inhibited neurite outgrowth. Although direct evidence is currently lacking, it was proposed that dysfunction of the ER?Golgi compartment in astrocytes overexpressing ??syn may lead to a decline of GDNF levels, which in turn would suppress neurite outgrowth. Taken together, the results of the present study offer further insights into the pathogenesis of PD from the perspective of astrocytes, which may provide novel strategies for the diagnosis and treatment of PD in the future.;In addition, Golgi fragmentation was observed in the process. On the other hand, it was also demonstrated, in a primary neuronal?astroglial co?culture system, that the overexpression of ??syn significantly decreased the levels of glia?derived neurotrophic factor (GDNF) and partly inhibited neurite outgrowth. Although direct evidence is currently lacking, it was proposed that dysfunction of the ER?Golgi compartment in astrocytes overexpressing ??syn may lead to a decline of GDNF levels, which in turn would suppress neurite outgrowth. Taken together, the results of the present study offer further insights into the pathogenesis of PD from the perspective of astrocytes, which may provide novel strategies for the diagnosis and treatment of PD in the future. |
About TF
| TF name : | GFAPGDNF |
| TF experiment: | Immunofluorescence,Immunoassay,Western blot, CHOP Knockdown,transfection,Immunostaining,flow cytometry,RNA-seq,siRNA, |
| TF experiment description: | In addition, Golgi fragmentation was observed in the process. On the other hand, it was also demonstrated, in a primary neuronal?astroglial co?culture system, that the overexpression of ??syn significantly decreased the levels of glia?derived neurotrophic factor (GDNF) and partly inhibited neurite outgrowth. Although direct evidence is currently lacking, it was proposed that dysfunction of the ER?Golgi compartment in astrocytes overexpressing ??syn may lead to a decline of GDNF levels, which in turn would suppress neurite outgrowth. Taken together, the results of the present study offer further insights into the pathogenesis of PD from the perspective of astrocytes, which may provide novel strategies for the diagnosis and treatment of PD in the future.;In addition, Golgi fragmentation was observed in the process. On the other hand, it was also demonstrated, in a primary neuronal?astroglial co?culture system, that the overexpression of ??syn significantly decreased the levels of glia?derived neurotrophic factor (GDNF) and partly inhibited neurite outgrowth. Although direct evidence is currently lacking, it was proposed that dysfunction of the ER?Golgi compartment in astrocytes overexpressing ??syn may lead to a decline of GDNF levels, which in turn would suppress neurite outgrowth. Taken together, the results of the present study offer further insights into the pathogenesis of PD from the perspective of astrocytes, which may provide novel strategies for the diagnosis and treatment of PD in the future.;In addition, Golgi fragmentation was observed in the process. On the other hand, it was also demonstrated, in a primary neuronal?astroglial co?culture system, that the overexpression of ??syn significantly decreased the levels of glia?derived neurotrophic factor (GDNF) and partly inhibited neurite outgrowth. Although direct evidence is currently lacking, it was proposed that dysfunction of the ER?Golgi compartment in astrocytes overexpressing ??syn may lead to a decline of GDNF levels, which in turn would suppress neurite outgrowth. Taken together, the results of the present study offer further insights into the pathogenesis of PD from the perspective of astrocytes, which may provide novel strategies for the diagnosis and treatment of PD in the future. |
About Function
| Enhancer function : | In addition, Golgi fragmentation was observed in the process. On the other hand, it was also demonstrated, in a primary neuronal?astroglial co?culture system, that the overexpression of ??syn significantly decreased the levels of glia?derived neurotrophic factor (GDNF) and partly inhibited neurite outgrowth. Although direct evidence is currently lacking, it was proposed that dysfunction of the ER?Golgi compartment in astrocytes overexpressing ??syn may lead to a decline of GDNF levels, which in turn would suppress neurite outgrowth. Taken together, the results of the present study offer further insights into the pathogenesis of PD from the perspective of astrocytes, which may provide novel strategies for the diagnosis and treatment of PD in the future. |
| Enhancer function experiment: | Immunohistochemical staining |
| Enhancer function experiment description: |
In addition, Golgi fragmentation was observed in the process. On the other hand, it was also demonstrated, in a primary neuronal?astroglial co?culture system, that the overexpression of ??syn significantly decreased the levels of glia?derived neurotrophic factor (GDNF) and partly inhibited neurite outgrowth. Although direct evidence is currently lacking, it was proposed that dysfunction of the ER?Golgi compartment in astrocytes overexpressing ??syn may lead to a decline of GDNF levels, which in turn would suppress neurite outgrowth. Taken together, the results of the present study offer further insights into the pathogenesis of PD from the perspective of astrocytes, which may provide novel strategies for the diagnosis and treatment of PD in the future. |
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