人 DDX58 抗体对
01AB03616
Antiviral innate immune response receptor RIG-I (RIGI) is a critical receptor in the innate immune response, primarily functioning as a pattern recognition receptor that detects viral RNA, particularly double-stranded RNA (dsRNA) and triphosphorylated RNA. RIGI is characterized by its unique structural domains, including two caspase activation and recruitment domains (CARDs), an RNA-dependent ATPase motor domain, and a carboxy-terminal domain (CTD). Upon binding to viral RNA, RIGI undergoes a conformational change that activates downstream signaling pathways through interaction with the mitochondrial antiviral signaling protein (MAVS), leading to the transcription of type I interferons (IFN-α and IFN-β) and other pro-inflammatory cytokines. Dysregulation of RIGI signaling is implicated in various diseases, including autoimmune disorders, where excessive activation can lead to tissue damage. Additionally, RIGI has been linked to cancer, as its activation can enhance anti-tumor immunity but may also contribute to tumor progression in certain contexts.
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技术参数
- 靶点基因名
- RIGI
- 基因别名
- DDX58
- 蛋白别名
- RNA sensor RIG-I; DDX58
- UniProt
- O95786
- 物种
- Human
产品详情
- 靶点名称
- DDX58
- 蛋白名称
- RNA sensor RIG-I
- 蛋白别名
- Antiviral innate immune response receptor RIG-I; ATP-dependent RNA helicase DDX58; DEAD box protein 58; RIG-I-like receptor 1; RLR-1; RNA sensor RIG-I; Retinoic acid-inducible gene 1 protein; RIG-1; Retinoic acid-inducible gene I protein; RIG-I
- 靶点基因名
- RIGI
- 基因别名
- DDX58
- UniProt
- O95786
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Antiviral innate immune response receptor RIG-I (RIGI) is a critical receptor in the innate immune response, primarily functioning as a pattern recognition receptor that detects viral RNA, particularly double-stranded RNA (dsRNA) and triphosphorylated RNA. RIGI is characterized by its unique structural domains, including two caspase activation and recruitment domains (CARDs), an RNA-dependent ATPase motor domain, and a carboxy-terminal domain (CTD). Upon binding to viral RNA, RIGI undergoes a conformational change that activates downstream signaling pathways through interaction with the mitochondrial antiviral signaling protein (MAVS), leading to the transcription of type I interferons (IFN-α and IFN-β) and other pro-inflammatory cytokines. Dysregulation of RIGI signaling is implicated in various diseases, including autoimmune disorders, where excessive activation can lead to tissue damage. Additionally, RIGI has been linked to cancer, as its activation can enhance anti-tumor immunity but may also contribute to tumor progression in certain contexts.