Lane 1: Mouse brain tissue lysate
Lane 2: Siha cell lysate
Lane 3: Mouse cerebellum tissue lysate
Lane 4: A431 cell lysate
Recombinant Rabbit monoclonal primary
CLSTN1 Recombinant Rabbit Monoclonal Antibody [JE48-81] (ET7109-84)
Recombinant protein within human clstn1 aa 860-981 / 981.
Mouse brain tissue lysate, Siha cell lysate, mouse cerebellum tissue lysate, A431 cell lysate, human liver cancer tissue, human kidney tissue.
Store at +4C after thawing. Aliquot store at -20C. Avoid repeated freeze / thaw cycles.
1*TBS (pH7.4), 0.05% BSA, 40% Glycerol. Preservative: 0.05% Sodium Azide.
Protein affinity purified.
Predicted band size: 110 kDa.
Alc alpha antibody; Alc-alpha antibody; Alcadein alpha 1 antibody; Alcadein alpha antibody; Alcadein-alpha antibody; alcalpha1 antibody; alcalpha2 antibody; Alzheimer related cadherin like protein antibody; Alzheimer-related cadherin-like protein antibody; C-terminal fragment 1-alpha antibody; Cadherin related family member 12 antibody; Calsyntenin 1 antibody; Calsyntenin1 antibody; CDHR12 antibody; CLSTN 1 antibody; Clstn1 antibody; CS1 antibody; CSTN1 antibody; CSTN1_HUMAN antibody; CTF1-alpha antibody; FLJ32258 antibody; KIAA0911 antibody; Non classical cadherin XB31alpha antibody; Non classical cadherin XB31alpha1 antibody; Non-classical cadherin XB31alpha antibody; PIK3CD antibody; SAlc-alpha antibody; XB31alpha antibody
Expressed in the brain and, a lower level, in the heart, skeletal muscle, kidney and placenta. Accumulates in dystrophic neurites around the amyloid core of Alzheimer disease senile plaques (at protein level).
Proteolytically processed under normal cellular conditions. A primary zeta-cleavage generates a large extracellular (soluble) N-terminal domain (sAlc) and a short C-terminal transmembrane fragment (CTF1). A secondary cleavage catalyzed by presenilin gamma-secretase within the transmembrane domain releases the beta-Alc-alpha chain in the extracellular milieu and produces an intracellular fragment (AlcICD). This processing is strongly suppressed in the tripartite complex formed with APBA2 and APP, which seems to prevent the association with PSEN1.
Endoplasmic reticulum. Golgi apparatus. Membrane. Nucleus.
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).