抗人 CAMSAP3 抗体对
01AB01034
Calmodulin regulated spectrin associated protein family member 3 (CAMSAP3) is a key microtubule-organizing protein that specifically binds to the minus-end of non-centrosomal microtubules, regulating their dynamics and organization within the cell. It enables both actin filament binding and microtubule minus-end binding activities, playing crucial roles in microtubule cytoskeleton organization, regulation of organelle positioning, and maintenance of cell-cell junctions such as the zonula adherens. CAMSAP3 is essential for the formation and polarity of basal bodies and the central pair of microtubules in motile cilia, influencing ciliary structure, synchronized beating, and overall function in multiciliated cells. Loss of CAMSAP3 disrupts these processes, leading to defects reminiscent of primary ciliary dyskinesia, including impaired mucociliary clearance, subfertility, and respiratory issues. Additionally, CAMSAP3 has been implicated in protecting lung carcinoma cells from epithelial-mesenchymal transition (EMT) by regulating microtubule dynamics and suppressing Akt activity. Diseases associated with CAMSAP3 mutations include autosomal dominant and recessive forms of deafness.
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技术参数
- 靶点基因名
- CAMSAP3
- 基因别名
- KIAA1543
- 蛋白别名
- calmodulin regulated spectrin associated protein family member 3; CAMSAP3
- UniProt
- Q9P1Y5
- 物种
- Human
产品详情
- 靶点名称
- CAMSAP3
- 蛋白名称
- calmodulin regulated spectrin associated protein family member 3
- 蛋白别名
- Calmodulin-regulated spectrin-associated protein 3; Protein Nezha
- 靶点基因名
- CAMSAP3
- 基因别名
- KIAA1543
- UniProt
- Q9P1Y5
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Calmodulin regulated spectrin associated protein family member 3 (CAMSAP3) is a key microtubule-organizing protein that specifically binds to the minus-end of non-centrosomal microtubules, regulating their dynamics and organization within the cell. It enables both actin filament binding and microtubule minus-end binding activities, playing crucial roles in microtubule cytoskeleton organization, regulation of organelle positioning, and maintenance of cell-cell junctions such as the zonula adherens. CAMSAP3 is essential for the formation and polarity of basal bodies and the central pair of microtubules in motile cilia, influencing ciliary structure, synchronized beating, and overall function in multiciliated cells. Loss of CAMSAP3 disrupts these processes, leading to defects reminiscent of primary ciliary dyskinesia, including impaired mucociliary clearance, subfertility, and respiratory issues. Additionally, CAMSAP3 has been implicated in protecting lung carcinoma cells from epithelial-mesenchymal transition (EMT) by regulating microtubule dynamics and suppressing Akt activity. Diseases associated with CAMSAP3 mutations include autosomal dominant and recessive forms of deafness.