Description
Product Characteristics:
Members of the calsyntenin protein family are localized to the post-synaptic membrane of exicitatory central nervous system (CNS) synapses. Calsyntenin-1, also known as CSTN1, PIK3CD, Alzheimer-related cadherin-like protein, non-classical cadherin XB31alpha, KIAA0911, ALC-ALPHA, alcalpha1, alcalpha2 or FLJ32258, is a 981 amino acid single-pass type I membrane protein that localizes to the membrane of endoplasmic reticulum, Golgi apparatus, cell projections and postsynaptic cells. Expressed in brain, calsyntenin-1 is also found at lower levels in placenta, skeletal muscle, heart and kidney. Calsyntenin-1 binds synaptic Ca2+ with its cytoplasmic domain and plays a role in extracellular proteolysis. Calsyntenin-1 is also known to form a complex with X11 Beta and APP to suppress the metabolic cleavage of APP, and docks vesicular cargo to KLC1. Calsyntenin-1 may be related to the development or progression of Alzheimer?s disease, and two calsyntenin-1 isoforms are produced as a result of alternative splicing events.
Subcellular location: Cytoplasm, Nucleus, Cell membrane
Synonyms: Alc alpha, Alc-alpha, Alcadein alpha 1, Alcadein alpha, Alcadein-alpha, alcalpha1, alcalpha2, Alzheimer related cadherin like protein, Alzheimer-related cadherin-like protein, Calsyntenin-1, Calsyntenin1, CLSTN 1, Clstn1, CS1, CSTN1, CSTN1_HUMAN, CTF1-alpha, FLJ32258, KIAA0911, Non classical cadherin XB31alpha, Non-classical cadherin XB31alpha, PIK3CD, SAlc-alpha, XB31alpha.
Target Information: Induces KLC1 association with vesicles and functions as a cargo in axonal anterograde transport. 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. 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. The intracellular fragment AlcICD suppresses APBB1-dependent transactivation stimulated by APP C-terminal intracellular fragment (AICD), most probably by competing with AICD for APBB1- binding. May modulate calcium-mediated postsynaptic signals (By similarity)