Overview
| 别名 | E3 ubiquitin ligase TRAF3IP2; Adapter protein CIKS; Connection to IKK and SAPK/JNK; E3 ubiquitin-protein ligase CIKS; Nuclear factor NF-kappa-B activator 1; ACT1; TRAF3-interacting protein 2 |
| 基因名 | TRAF3IP2 |
| UniProt ID | O43734 |
| 反应种属 | Human |
| 应用 | WB |
| 宿主 | Mouse |
| 偶联物 | Unconjugated |
| 修饰 | Unmodified |
| 亚型 | IgG2a |
| 克隆号 | 9Q6-J6-A9 |
| 克隆性 | Monoclonal Antibody |
| 分子量 | Calculated MW: 64 kDa |
| 纯化方式 | Affinity Purified |
| 产品形式 | Liquid |
| 推荐稀释比 | WB-1:1000 |
| 存储缓冲液 | Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.09% sodium azide |
| 保存温度 | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
| 背景信息 | TRAF3 interacting protein 2 (TRAF3IP2), also known as ACT1 or CIKS, is a cytoplasmic adaptor and E3 ubiquitin ligase that mediates Lys63-linked polyubiquitination to facilitate protein-protein interactions. It is a central component of the IL-17A signaling pathway, where it binds to IL17RA/RC receptors via SEFIR domains and recruits TRAF6 to activate canonical NF-kappaB and MAPK pathways. This signaling is vital for regulating cytokine responses in innate and adaptive immunity. Clinically, germline variants in TRAF3IP2 are associated with psoriasis 13 and psoriatic arthritis, driven by dysregulated IL-17 signaling. Furthermore, loss-of-function mutations cause familial candidiasis 8 due to impaired antifungal immunity, while experimental evidence also links the protein to vascular insulin resistance and hypertension. |
检测原理