Anti-Human CLSTN1 Antibody Pair

Product Description: 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. Protein Function: Postsynaptic adhesion molecule that binds to presynaptic neurexins to mediate both excitatory and inhibitory synapse formation (By similarity). Promotes synapse development by acting as a cell adhesion molecule at the postsynaptic membrane, which associates with neurexin-alpha at the presynaptic membrane (By similarity). Also functions as a cargo in axonal anterograde transport by acting as a molecular adapter that promotes KLC1 association with vesicles (PubMed:21385839). Complex formation with APBA2 and APP, stabilizes APP metabolism and enhances APBA2-mediated suppression of beta-APP40 secretion, due to the retardation of intracellular APP maturation (PubMed:12972431) , As intracellular fragment AlcICD, suppresses APBB1-dependent transactivation stimulated by APP C-terminal intracellular fragment (AICD), most probably by competing with AICD for APBB1-binding (PubMed:15037614) , In complex with APBA2 and C99, a C-terminal APP fragment, abolishes C99 interaction with PSEN1 and thus APP C99 cleavage by gamma-secretase, most probably through stabilization of the direct interaction between APBA2 and APP (PubMed:15037614) [The Uniprot Consortium]