抗人 CFAP45 抗体对
01AB02387
Cilia and flagella associated protein 45 (CFAP45) is a cytoskeletal protein integral to the axonemal structure of motile cilia and flagella, where it interacts with dynein ATPases and adenylate kinase to regulate adenine nucleotide homeostasis, particularly by binding AMP and facilitating microtubule sliding necessary for effective ciliary and flagellar beating. CFAP45 contains domains that enable stable three-dimensional folding and specific interactions with other proteins, contributing to its role in the axonemal module that controls motility. Deficiency of CFAP45 in humans and mice leads to a motile ciliopathy characterized by normal ciliary morphology but impaired function, manifesting clinically as situs inversus totalis and asthenospermia due to dyskinetic beating of nodal cilia and sperm flagella. Restoration of nucleotide balance with AMP or ADP can rescue the motility defect, highlighting CFAP45’s essential role in maintaining proper ciliary and flagellar movement.
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技术参数
- 靶点基因名
- CFAP45
- 基因别名
- CCDC19; NESG1
- 蛋白别名
- cilia and flagella associated protein 45; CFAP45
- UniProt
- Q9UL16
- 物种
- Human
产品详情
- 靶点名称
- CFAP45
- 蛋白名称
- cilia and flagella associated protein 45
- 蛋白别名
- Cilia- and flagella-associated protein 45; Coiled-coil domain-containing protein 19; Nasopharyngeal epithelium-specific protein 1
- 靶点基因名
- CFAP45
- 基因别名
- CCDC19; NESG1
- UniProt
- Q9UL16
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Cilia and flagella associated protein 45 (CFAP45) is a cytoskeletal protein integral to the axonemal structure of motile cilia and flagella, where it interacts with dynein ATPases and adenylate kinase to regulate adenine nucleotide homeostasis, particularly by binding AMP and facilitating microtubule sliding necessary for effective ciliary and flagellar beating. CFAP45 contains domains that enable stable three-dimensional folding and specific interactions with other proteins, contributing to its role in the axonemal module that controls motility. Deficiency of CFAP45 in humans and mice leads to a motile ciliopathy characterized by normal ciliary morphology but impaired function, manifesting clinically as situs inversus totalis and asthenospermia due to dyskinetic beating of nodal cilia and sperm flagella. Restoration of nucleotide balance with AMP or ADP can rescue the motility defect, highlighting CFAP45’s essential role in maintaining proper ciliary and flagellar movement.