Home Details
| Official Symbol of Gene | Tnf |
| Species | Mus musculus |
| Entrez Gene ID | 21926 |
| Official Full Name | tumor necrosis factor |
| Also known as | DIF; Tnfa; TNF-a; TNFSF2; Tnlg1f; Tnfsf1a; TNFalpha; TNF-alpha |
| Gene Type | protein coding |
| dbXrefs | Ensembl:ENSMUSG00000024401 AllianceGenome:MGI:104798 |
| Map Location | 17 B1; 17 18.59 cM |
| Detected Sample | brain |
| Sample Detail | microglia |
| Detected Method | Western blot analysis |
| Disease | inflammatory effects |
| Disease subtype | cerebral ischemia, multiple sclerosis, and Alzheimer’s disease |
| Population | immortalized murine BV2 microglial cell |
| Sample Size | N/A |
| Pubmed ID | 24244819 |
| Year | 2013 |
| Title | Kalopanaxsaponin A Exerts Anti-Inflammatory Effects in Lipopolysaccharide-Stimulated Microglia via Inhibition of JNK and NF-κB/AP-1 Pathways |
| Expression | up-regulation |
| Risk type | Disease risk |
| Result | we showed that kalopanaxsaponin A, a triterpenoid saponin isolated from Kalopanax pictus, inhibited inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and tumor necrosis factor (TNF)-α expression in lipopolysaccharide (LPS)-stimulated microglia, while kalopanaxsaponin A increased anti-infl ammatory cytokine interleukin (IL)-10 expression. Subsequent mechanistic studies revealed that kalopanaxsaponin A inhibited LPS-induced DNA binding activities of NF-κB and AP-1, and the phosphorylation of JNK without affecting other MAP kinases. Furthermore, kalopanaxsaponin A inhibited the intracellular ROS production with upregulation of anti-infl ammatory hemeoxygenase-1 (HO-1) expression. Based on the previous reports that JNK pathway is largely involved in iNOS and proinfl ammatory cytokine gene expression via modulating NF-κB/AP-1 and ROS, our data collectively suggest that inhibition of JNK pathway plays a key role in anti-infl ammatory effects of kalopanaxsaponin A in LPS-stimulated microglia |
| Mechanism/Pathway | JNK pathway is largely involved in iNOS and proinfl ammatory cytokine gene expression via modulating NF-κB/AP-1 and ROS |

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