Cell Signaling Technology

Product Pathways - Neuroscience

SynGAP Antibody #3200

Applications Reactivity Sensitivity MW (kDa) Source
W M R (H) Endogenous 140 Rabbit

Applications Key:  W=Western Blotting
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 Antibody detects endogenous levels of total SynGAP protein.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to human SynGAP. Antibodies are purified by peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from mouse and rat brain tissue using SynGAP Antibody.

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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