Cell Signaling Technology

Product Pathways - Neuroscience

SynGAP (D78B11) Rabbit mAb #5540

Applications Reactivity Sensitivity MW (kDa) Isotype
W IP M R (H) Endogenous 140 Rabbit IgG

Applications Key:  W=Western Blotting  IP=Immunoprecipitation
Reactivity Key:  H=Human  M=Mouse  R=Rat
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

SynGAP (D78B11) Rabbit mAb detects endogenous levels of total SynGAP protein.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide surrounding Arg710 of human SynGAP protein.

Western Blotting

Western Blotting

Western blot analysis of extracts from mouse and rat brain using SynGAP (D78B11) Rabbit mAb.

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).

  1. Kim, J.H. et al. (1998) Neuron 20, 683-91.
  2. Oh, J.S. et al. (2004) J Biol Chem 279, 17980-8.
  3. Krapivinsky, G. et al. (2004) Neuron 43, 563-74.
  4. Song, B. et al. (2004) Brain Res 1005, 44-50.
  5. Komiyama, N.H. et al. (2002) J Neurosci 22, 9721-32.
  6. Kim, J.H. et al. (2003) J Neurosci 23, 1119-24.

Application References

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Companion Products

For Research Use Only. Not For Use In Diagnostic Procedures.

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