CLSTN1 Recombinant Rabbit mAb (一抗) - WB,IHC-P,IHC-F,IF,Flow-Cyt | Bioss

bsm-62063R

重组兔单抗

CLSTN1 Recombinant Rabbit mAb

老年痴呆相关类钙粘蛋白CS1重组兔单抗

ALC-ALPHA; CDHR12; CST-1; CSTN1; PIK3CD; XB31alpha; alcalpha1; alcalpha2; 1810034E21Rik; CSTN1_HUMAN; CLSTN1; Alcadein-alpha (Alc-alpha); Alzheimer-related cadherin-like protein; Non-classical cadherin XB31alpha; CS1; KIAA0911; CSTN1_MOUSE; calsyntenin 1; cadherin-related family member 12

Rabbit

A synthesized peptide derived from human Calsyntenin 1: 920-981/981

IgG

Liquid

affinity purified by Protein A

Recombinant

4A11

110 kDa

145 kDa

10mM phosphate buffered saline(pH 7.4) with 150mM sodium chloride, 0.05% BSA, 0.02% Proclin300 and 50% glycerol.

Store at 4℃ for short term. Store at -20℃ for long term. Avoid repeated freeze/thaw cycles.

This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.

Postsynaptic adhesion molecule that binds to presynaptic neurexins to mediate both excitatory and inhibitory synapse formation. Promotes synapse development by acting as a cell adhesion molecule at the postsynaptic membrane, which associates with neurexin-alpha at the presynaptic membrane.

CLSTN1

Calsyntenin-1

Directly interacts with APBA2. Forms a tripartite complex with APBA2 and APP. The CTF1 chain interacts with PSEN1. The intracellular fragment AlcICD interacts with APBB1; this interaction stabilizes AlcICD metabolism. Interacts with KLC1 and APBB1

Endoplasmic reticulum membrane. Golgi apparatus membrane. Cell projection. Cell junction > synapse > postsynaptic cell membrane. Nucleus. Neurite tips. Localized in the postsynaptic membrane of both excitatory and inhibitory synapses (By similarity). The AlcICD fragment is translocated to the nucleus upon interaction with APBB1.

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.

Contains 2 cadherin domains.

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.