About Enhancer
| Enhancer ID: | E_01_0427 |
| Species: | mouse |
| Position : | chr14:51429786-51431786   |
| Biosample name: | |
| Experiment class : | High+Lowthroughput |
| Enhancer type: | Enhancer |
| Disease: | Rheumatoid arthritis (ra) |
| Pubmed ID: | 29879032 |
| Enhancer experiment: | MTT,Flow cytometry,Western blot |
| Enhancer experiment description: | Initially, we found that BAY11-7082 inhibited NF-?B expression in a concentration-dependent manner. According to the findings of MTT assay and flow cytometry, we understood that RA-HFLS treated by BAY11-7082 (an inhibitor of NF-?B), the inhibition of NF-?B pathway, suppressed RA-HFLS proliferation and induced RA-HFLS apoptosis in a concentration and time-dependent manner. Furthermore, RA-HFLS treated by BAY11-7082 presented decreased VEGF, Ang1 and Ang2 expressions in a concentration-dependent manner.The study concluded that inhibition of NF-?B pathway induced cell apoptosis and suppressed proliferation and angiogenesis of RA-HFLS, which could serve as a novel target in the treatment of RA. |
About Target gene
| Target gene : | Ang2(Angrp,Raa3,Rnase5b) |
| Strong evidence: | qRT-PCR,qPCR,ChIP,3C |
| Less strong evidence: | RNA-Seq |
| Target gene experiment description: | Initially, we found that BAY11-7082 inhibited NF-?B expression in a concentration-dependent manner. According to the findings of MTT assay and flow cytometry, we understood that RA-HFLS treated by BAY11-7082 (an inhibitor of NF-?B), the inhibition of NF-?B pathway, suppressed RA-HFLS proliferation and induced RA-HFLS apoptosis in a concentration and time-dependent manner. Furthermore, RA-HFLS treated by BAY11-7082 presented decreased VEGF, Ang1 and Ang2 expressions in a concentration-dependent manner.The study concluded that inhibition of NF-?B pathway induced cell apoptosis and suppressed proliferation and angiogenesis of RA-HFLS, which could serve as a novel target in the treatment of RA. |
About TF
| TF name : | -- |
| TF experiment: | MTT,Flow cytometry,Western blot |
| TF experiment description: | Initially, we found that BAY11-7082 inhibited NF-?B expression in a concentration-dependent manner. According to the findings of MTT assay and flow cytometry, we understood that RA-HFLS treated by BAY11-7082 (an inhibitor of NF-?B), the inhibition of NF-?B pathway, suppressed RA-HFLS proliferation and induced RA-HFLS apoptosis in a concentration and time-dependent manner. Furthermore, RA-HFLS treated by BAY11-7082 presented decreased VEGF, Ang1 and Ang2 expressions in a concentration-dependent manner.The study concluded that inhibition of NF-?B pathway induced cell apoptosis and suppressed proliferation and angiogenesis of RA-HFLS, which could serve as a novel target in the treatment of RA. |
About Function
| Enhancer function : | Initially, we found that BAY11-7082 inhibited NF-?B expression in a concentration-dependent manner. According to the findings of MTT assay and flow cytometry, we understood that RA-HFLS treated by BAY11-7082 (an inhibitor of NF-?B), the inhibition of NF-?B pathway, suppressed RA-HFLS proliferation and induced RA-HFLS apoptosis in a concentration and time-dependent manner. Furthermore, RA-HFLS treated by BAY11-7082 presented decreased VEGF, Ang1 and Ang2 expressions in a concentration-dependent manner.The study concluded that inhibition of NF-?B pathway induced cell apoptosis and suppressed proliferation and angiogenesis of RA-HFLS, which could serve as a novel target in the treatment of RA. |
| Enhancer function experiment: | Immunohistochemical staining |
| Enhancer function experiment description: |
Initially, we found that BAY11-7082 inhibited NF-?B expression in a concentration-dependent manner. According to the findings of MTT assay and flow cytometry, we understood that RA-HFLS treated by BAY11-7082 (an inhibitor of NF-?B), the inhibition of NF-?B pathway, suppressed RA-HFLS proliferation and induced RA-HFLS apoptosis in a concentration and time-dependent manner. Furthermore, RA-HFLS treated by BAY11-7082 presented decreased VEGF, Ang1 and Ang2 expressions in a concentration-dependent manner.The study concluded that inhibition of NF-?B pathway induced cell apoptosis and suppressed proliferation and angiogenesis of RA-HFLS, which could serve as a novel target in the treatment of RA. |
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