PathScan® RP SynGAP Sandwich ELISA Kit #57320
Filter:
- ELISA
Supporting Data
REACTIVITY | H M R |
Application Key:
- ELISA-ELISA
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
Product Information
Product Description
The rapid protocol (RP) PathScan® RP SynGAP Sandwich ELISA Kit is a solid phase sandwich enzyme-linked immunosorbent assay (ELISA) that detects endogenous levels of SynGAP protein in a reduced assay time of 1.5 hours. Incubation of cell lysates and detection antibody on the coated microwell plate forms a sandwich with SynGAP in a single step. The plate is then extensively washed and TMB reagent is added for signal development. The magnitude of absorbance for the developed color is proportional to the quantity of SynGAP protein. Learn more about your ELISA kit options here.
*Antibodies in this kit are custom formulations specific to kit.
*Antibodies in this kit are custom formulations specific to kit.
Protocol
Specificity / Sensitivity
The PathScan® RP SynGAP Sandwich ELISA Kit detects endogenous levels of SynGAP protein. The kit sensitivity is shown in Figure 1. This kit detects proteins from the indicated species, as determined through in-house testing, but may also detect homologous proteins from other species.
Species Reactivity:
Human, Mouse, Rat
Background
SynGAP is a synaptic GTPase-activating protein selectively expressed in the brain and found at higher concentrations, specifically at excitatory synapses in the mammalian forebrain. SynGAP has a PH domain, a C2 domain, and a highly conserved RasGAP domain, which negatively regulates both Ras activity and its downstream signaling pathways. SynGAP interacts with the PDZ domains of SAP102, as well as PSD95, a postsynaptic scaffolding protein that couples SynGAP to NMDA receptors (1). SynGAP is phosphorylated by Ca2+/calmodulin-dependent protein kinase II (CaMKII) at Ser765 and Ser1123, among other sites (2,3). Phosphorylation of SynGAP results in stimulation of the GTPase activity of Ras, and PSD95-dependent CaMKII phosphorylation of SynGAP increases after transient brain ischemia (1,4). SynGAP is implicated in NMDAR- and CaMKII-dependent regulation of AMPAR trafficking and plays an important role in synaptic plasticity (3,5). SynGAP is critical during neuronal development as mice lacking SynGAP protein die postnatally. Furthermore, SynGAP mutant mice have reduced long-term potentiation (LTP) and perform poorly in spatial memory tasks (6).
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For Research Use Only. Not For Use In Diagnostic Procedures.
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