人 STAT2 抗体对
01AB03690
Signal transducer and activator of transcription 2 (STAT2) is a critical transcription factor that mediates cellular responses to type I and type III interferons (IFNs). Upon activation by these cytokines, STAT2 forms a heterodimer with STAT1 and the interferon regulatory factor 9 (IRF9), collectively known as the IFN-stimulated gene factor 3 (ISGF3). This complex translocates to the nucleus, where it binds to interferon-stimulated response elements (ISREs) in the DNA, initiating the transcription of genes involved in antiviral responses and immune regulation. Dysregulation of STAT2 has been linked to various diseases, particularly immunodeficiencies. Mutations in the STAT2 gene can lead to severe susceptibility to viral infections, as seen in patients with homozygous mutations resulting in a loss of function. Additionally, gain-of-function mutations have been associated with autoinflammatory syndromes characterized by excessive type I IFN signaling.
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技术参数
- 靶点基因名
- STAT2
- 蛋白别名
- signal transducer and activator of transcription 2; STAT2
- UniProt
- P52630
- 物种
- Human
产品详情
- 靶点名称
- STAT2
- 蛋白名称
- signal transducer and activator of transcription 2
- 蛋白别名
- Signal transducer and activator of transcription 2; p113
- 靶点基因名
- STAT2
- UniProt
- P52630
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Signal transducer and activator of transcription 2 (STAT2) is a critical transcription factor that mediates cellular responses to type I and type III interferons (IFNs). Upon activation by these cytokines, STAT2 forms a heterodimer with STAT1 and the interferon regulatory factor 9 (IRF9), collectively known as the IFN-stimulated gene factor 3 (ISGF3). This complex translocates to the nucleus, where it binds to interferon-stimulated response elements (ISREs) in the DNA, initiating the transcription of genes involved in antiviral responses and immune regulation. Dysregulation of STAT2 has been linked to various diseases, particularly immunodeficiencies. Mutations in the STAT2 gene can lead to severe susceptibility to viral infections, as seen in patients with homozygous mutations resulting in a loss of function. Additionally, gain-of-function mutations have been associated with autoinflammatory syndromes characterized by excessive type I IFN signaling.