人 TRAF3IP2 抗体对
01AB02701
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.
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技术参数
- 靶点基因名
- TRAF3IP2
- 基因别名
- C6orf2; C6orf4; C6orf5; C6orf6
- 蛋白别名
- TRAF3 interacting protein 2; TRAF3IP2
- UniProt
- O43734
- 物种
- Human
产品详情
- 靶点名称
- TRAF3IP2
- 蛋白名称
- TRAF3 interacting protein 2
- 蛋白别名
- 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
- 靶点基因名
- TRAF3IP2
- 基因别名
- C6orf2; C6orf4; C6orf5; C6orf6
- UniProt
- O43734
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
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.