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CLSTN1 Antibody (N-term) Blocking Peptide
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
| Primary Accession | O94985 |
|---|---|
| Clone Names | 110826086 |
| 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 | Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed. |
| Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C. |
| Precautions | This product is for research use only. Not for use in diagnostic or therapeutic procedures. |
| Name | CLSTN1 (HGNC:17447) |
|---|---|
| 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). |
| Cellular Location | Postsynaptic cell membrane {ECO:0000250|UniProtKB:Q9EPL2}; Single-pass type I membrane protein. Endoplasmic reticulum membrane; Single-pass type I membrane protein. Golgi apparatus membrane; Single-pass type I membrane protein. Cell projection, neuron projection. Note=Localized in the postsynaptic membrane of both excitatory and inhibitory synapses {ECO:0000250|UniProtKB:Q9EPL2} |
| 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). |
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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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