抗人 CLSTN1 抗体对
01AB00775
Calsyntenin 1 (CLSTN1), also known as alcadein-alpha, is a type I transmembrane protein predominantly expressed in the nervous system and plays a critical role in neuronal development and function. It acts as a cell adhesion molecule at the postsynaptic membrane, promoting synapse development by interacting with neurexin-alpha at the presynaptic site and binding to kinesin-1 motors to mediate axonal anterograde transport of specific vesicles and proteins, including the amyloid precursor protein (APP). CLSTN1 is essential for axon branching and neuronal compartmentalization, regulating the trafficking of Rab5-containing endosomes and influencing the formation of peripheral sensory axons. It also binds calcium ions and participates in protein-protein interactions, including with APBA2 and APP. Clinically, mutations or dysregulation of CLSTN1 have been implicated in the pathogenic mechanisms of Alzheimer’s disease, likely due to its role in APP processing and synaptic maintenance.
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技术参数
- 靶点基因名
- CLSTN1
- 基因别名
- CS1; KIAA0911
- 蛋白别名
- calsyntenin 1; CLSTN1
- UniProt
- O94985
- 物种
- Human
产品详情
- 靶点名称
- CLSTN1
- 蛋白名称
- calsyntenin 1
- 蛋白别名
- Calsyntenin-1; Alcadein-alpha; Alc-alpha; Alzheimer-related cadherin-like protein; Non-classical cadherin XB31alpha) [Cleaved into: Soluble Alc-alpha; SAlc-alpha; CTF1-alpha; C-terminal fragment 1-alpha]
- 靶点基因名
- CLSTN1
- 基因别名
- CS1; KIAA0911
- UniProt
- O94985
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Calsyntenin 1 (CLSTN1), also known as alcadein-alpha, is a type I transmembrane protein predominantly expressed in the nervous system and plays a critical role in neuronal development and function. It acts as a cell adhesion molecule at the postsynaptic membrane, promoting synapse development by interacting with neurexin-alpha at the presynaptic site and binding to kinesin-1 motors to mediate axonal anterograde transport of specific vesicles and proteins, including the amyloid precursor protein (APP). CLSTN1 is essential for axon branching and neuronal compartmentalization, regulating the trafficking of Rab5-containing endosomes and influencing the formation of peripheral sensory axons. It also binds calcium ions and participates in protein-protein interactions, including with APBA2 and APP. Clinically, mutations or dysregulation of CLSTN1 have been implicated in the pathogenic mechanisms of Alzheimer’s disease, likely due to its role in APP processing and synaptic maintenance.