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Induces KLC1 association with vesicles and functions as a cargo in axonal anterograde transport. Additionally we are shipping Calsyntenin 1 Antibodies (56) and Calsyntenin 1 Proteins (14) and many more products for this protein.
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Our results suggest a model in which Clstn-1 patterns separate axonal compartments and define their ability to branch by directing trafficking of specific endosomes.
These results indicate that regulated intramembrane proteolysis of Alca by gamma-secretase regulates APP (show APP ELISA Kits) trafficking and the production of Abeta (show APP ELISA Kits) in vivo.
these results highlight a key role for calsyntenin-1 in the transport of NMDA receptors to synaptic targets, which is necessary for the maturation of neuronal circuits during early development.
Alcalpha is efficiently processed in part to minimize the inappropriate peripheral retention of kinesin-1
Immunoisolated calsyntenin-1 organelles from murine brain homogenates; determined their proteome by MS. Found calsyntenin-1 organelles are endowed with components of the endosomal trafficking machinery and contained the beta-amyloid precursor protein (APP).
Phosphorylation of KLC1 (show KLC1 ELISA Kits) at serine 460 modulates binding and trafficking of calsyntenin-1.
Calsyntenin-1 links a certain type of vesicular and tubulovesicular organelles to the Kinesin-1 motor.
The novel cargo Alcadein induces vesicle association of kinesin-1 motor components and activates axonal transport.
Results suggests that APP (show APP ELISA Kits) partially compensates for defective Alcalpha in anterograde transport by providing an alternative cargo receptor for kinesin-1.
Calsyntenin-1 contributes to the early stages of the hepatitis C virus replication cycle and the formation of the replication complex.
Increased plasma p3-Alcalpha35, a major fragment of alcalpha1, may indicate an endophenotype in Alzheimer's disease patients with progressive cognitive impairment.
Increased plasma p3-alcadein (alc) alpha, evident in the early stages of cognitive impairment, suggests that alc metabolites are useful plasma biomarkers of Alzheimer's disease.
findings show that calsyntenin-1 is reduced in Alzheimer's disease brains and that the extent of this reduction correlates with increased amyloid-beta
CLSTN1 is a target gene of the BACH1 (show BACH1 ELISA Kits) transcription factor according to ChIP-seq analysis in HEK (show EPHA3 ELISA Kits) 293 cells.
Alcadein and amyloid beta-protein precursor regulates FE65 (show APBB1 ELISA Kits)-dependent gene transactivation [alcalpha1, alcbeta (show CLSTN3 ELISA Kits), alcgamma (show CLSTN2 ELISA Kits)]
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).
, calsyntenin 1
, calsyntenin 3
, alcadein alpha
, alcadein alpha 1
, alzheimer-related cadherin-like protein
, cadherin-related family member 12
, non-classical cadherin XB31alpha
, non-classical cadherin XB31alpha1