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CLSTN1 Antibody (N-term) Blocking Peptide

Synthetic peptide

     
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Product Information
Primary Accession O94985
Clone Names 110826086
Peptide ID 110826086
Additional Information
Gene ID 22883
Other Names Calsyntenin-1, Alcadein-alpha, Alc-alpha, Alzheimer-related cadherin-like protein, Non-classical cadherin XB31alpha, Soluble Alc-alpha, SAlc-alpha, CTF1-alpha, C-terminal fragment 1-alpha, CLSTN1, CS1, KIAA0911
Format Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.
StorageMaintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.
PrecautionsThis product is for research use only. Not for use in diagnostic or therapeutic procedures.
Protein Information
Name CLSTN1
Synonyms CS1, KIAA0911
Function 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).
Cellular Location Endoplasmic reticulum membrane; Single-pass type I membrane protein. Golgi apparatus membrane. Cell projection. Cell junction, synapse, postsynaptic cell membrane; Single-pass type I membrane protein. Nucleus. Note=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.
Tissue Location 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).
Research Areas
Citations (0)

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Background

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).

References

Konecna, A., et al. Mol. Biol. Cell 17(8):3651-3663(2006)Wang, A.G., et al. Biochem. Biophys. Res. Commun. 345(3):1022-1032(2006)Araki, Y., et al. J. Biol. Chem. 279(23):24343-24354(2004)Schmitt-Ulms, G., et al. Nat. Biotechnol. 22(6):724-731(2004)Araki, Y., et al. J. Biol. Chem. 278(49):49448-49458(2003)

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$ 80.00
Cat# BP18952a
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