Human SYNPO(Synaptopodin) ELISA Kit (E-EL-H2013)

This ELISA kit uses the Sandwich-ELISA principle. The micro ELISA plate provided in this kit has been pre-coated with an antibody specific to Human SYNPO. Standards or samples are added to the micro ELISA plate wells and combined with the specific antibody. Then a biotinylated detection antibody specific for Human SYNPO and Avidin-Horseradish Peroxidase (HRP) conjugate are added successively to each micro plate well and incubated. Free components are washed away. The substrate solution is added to each well. Only those wells that contain Human SYNPO, biotinylated detection antibody and Avidin-HRP conjugate will appear blue in color. The enzyme-substrate reaction is terminated by the addition of stop solution and the color turns yellow. The optical density (OD) is measured spectrophotometrically at a wavelength of 450 nm ± 2 nm. The OD value is proportional to the concentration of Human SYNPO. You can calculate the concentration of Human SYNPO in the samples by comparing the OD of the samples to the standard curve.

Synaptopodin is an actin-associated protein that participates in regulating the morphology and motility of dendritic spines and of renal podocyte foot processes. It exists as two isoforms generated by alternative splicing, a neuronal form of the telencephalon and a renal form, and is highly enriched in the postsynaptic compartment of excitatory neurons and in glomerular podocyte foot processes, two structures that depend on dynamic actin remodeling. Synaptopodin contributes to the formation of the spine apparatus involved in synaptic plasticity, organizes the actin cytoskeleton through Rho family signaling pathways and stabilizes filamentous actin, thereby supporting the structural plasticity underlying strengthening and weakening of synaptic connections and the expression of long-term potentiation. In podocytes it maintains the foot-process architecture and stress-fiber organization required for the integrity of the glomerular filtration barrier. Loss of synaptopodin is associated with impaired synaptic plasticity, deficits in learning and spatial memory and reduced stress resilience, whereas its disappearance from the kidney is a recognized feature of podocyte injury in proteinuric glomerular disease. Measurement of synaptopodin supports research on neuronal cytoskeletal dynamics, synapse and memory function, podocyte biology and the evaluation of therapies aimed at protecting synaptic and renal structure.