Cell Signaling Technology

Product Pathways - Neuroscience

EAAT3 Antibody #12179

Applications Reactivity Sensitivity MW (kDa) Source
W IP H M R (Mk) Endogenous 70 Rabbit

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

Protocols

Specificity / Sensitivity

EAAT3 Antibody recognizes endogenous levels of total EAAT3 protein.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human EAAT3 protein. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from mouse brain, rat brain, and rat prefrontal cortex using EAAT3 Antibody.

IP

IP

Immunoprecipitation of EAAT3 from HeLa cell extracts, using Normal Rabbit IgG #2729 (lane 2) or EAAT3 Antibody (lane 3). Lane 1 is 10% input. Western blot analysis was performed using EAAT3 Antibody.

Background

During neurotransmission, glutamate is released from vesicles of the presynaptic cell, and glutamate receptors (e.g., NMDA Receptor, AMPA Receptor) bind glutamate for activation at the opposing postsynaptic cell. Excitatory amino acid transporters (EAATs) regulate and maintain extracellular glutamate concentrations below excitotoxic levels (1,2). In addition, glutamate transporters may limit the duration of synaptic excitation by an electrogenic process in which the transmitter is cotransported with three sodium ions and one proton, followed by countertransport of a potassium ion (1,2). Five EAATs (EAAT1-5) have been identified. EAAT1 and EAAT2 are expressed mainly in glia, while EAAT3, EAAT4, and EAAT5 are considered to be neuronal transporters (2). EAAT3 is found in the perisynaptic areas and cell bodies of glutamatergic and GABAergic neurons (3). Research studies have implicated abnormal EAAT3 expression in the pathophysiology of Schizophrenia (4,5).

  1. Danbolt, N.C. (2001) Prog Neurobiol 65, 1-105.
  2. Amara, S.G. and Fontana, A.C. (2002) Neurochem Int 41, 313-8.
  3. Rothstein, J.D. et al. (1994) Neuron 13, 713-25.
  4. Bauer, D. et al. (2008) Schizophr Res 104, 108-20.
  5. Horiuchi, Y. et al. (2012) Am J Med Genet B Neuropsychiatr Genet 159B, 30-7.

Application References

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

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