抗人 RANGRF 抗体对
01AB03008
RAN guanine nucleotide release factor (RANGRF), also known as MOG1, is a small nuclear protein that regulates the RAN GTPase cycle. Unlike classical guanine nucleotide exchange factors, RANGRF structurally binds RAN to promote guanine nucleotide release, thereby modulating the pool of GTP-bound RAN essential for nuclear transport and mitotic spindle assembly. It is a soluble, non-enzymatic regulator ubiquitously expressed in human tissues. Beyond its role in cellular trafficking, RANGRF is critical for cardiac physiology. It facilitates the surface expression of the cardiac sodium channel NaV1.5 (SCN5A). Loss-of-function variants in RANGRF impair this trafficking process, leading to reduced sodium current and are associated with cardiac conduction diseases, including Brugada syndrome and other arrhythmia phenotypes.
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技术参数
- 靶点基因名
- RANGRF
- 基因别名
- MOG1; RANGNRF
- 蛋白别名
- RAN guanine nucleotide release factor; RANGRF
- UniProt
- Q9HD47
- 物种
- Human
产品详情
- 靶点名称
- RANGRF
- 蛋白名称
- RAN guanine nucleotide release factor
- 蛋白别名
- Ran guanine nucleotide release factor; RanGNRF; Ran-binding protein MOG1
- 靶点基因名
- RANGRF
- 基因别名
- MOG1; RANGNRF
- UniProt
- Q9HD47
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
RAN guanine nucleotide release factor (RANGRF), also known as MOG1, is a small nuclear protein that regulates the RAN GTPase cycle. Unlike classical guanine nucleotide exchange factors, RANGRF structurally binds RAN to promote guanine nucleotide release, thereby modulating the pool of GTP-bound RAN essential for nuclear transport and mitotic spindle assembly. It is a soluble, non-enzymatic regulator ubiquitously expressed in human tissues. Beyond its role in cellular trafficking, RANGRF is critical for cardiac physiology. It facilitates the surface expression of the cardiac sodium channel NaV1.5 (SCN5A). Loss-of-function variants in RANGRF impair this trafficking process, leading to reduced sodium current and are associated with cardiac conduction diseases, including Brugada syndrome and other arrhythmia phenotypes.