Slc1a2 Rabbit Polyclonal Antibody

CAT#: TA328838

Rabbit Polyclonal Anti-Excitatory Amino Acid Transporter 2 (extracellular)

Product Images

Western blot analysis of rat cerebellum lysate: 1. Anti-Excitatory Amino Acid Transporter 2 (extracellular) antibody, (1:500). 2. Anti-Excitatory Amino Acid Transporter 2 (extracellular) antibody, preincubated with the control peptide antigen.

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  Western blot analysis of mouse brain membranes: 1. Anti-Excitatory Amino Acid Transporter 2 (extracellular) antibody, (1:200). 2. Anti-Excitatory Amino Acid Transporter 2 (extracellular) antibody, preincubated with the control peptide antigen.

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  Expression of EAAT2 in rat hippocampus. Immunohistochemical staining of perfusion-fixed, free floating frozen rat brain sections with Anti-Excitatory Amino Acid Transporter 2 (extracellular) antibody. In the rat hippocampal CA1 region EAAT2 immunoreactivity (green) appears in the neuropil in the stratum oriens (S. Or) and in the pyramidal layer (Pyr) and was particularly intense around pyramidal neurons (arrow in A and compare with DAPI counterstain in B).

Specifications

Product Data

• Applications: IHC, WB
• Recommended Dilution: WB: 1:200-1:2000; IHC: 1:100-1:3000
• Reactivities: Human, Mouse, Rat
• Host: Rabbit
• Clonality: Polyclonal
• Immunogen: Peptide (C)KQLGPGKKNDEVS, corresponding to amino acid residues 151-163 of rat EAAT2. 2nd extracellular loop.
• Formulation: Lyophilized. Concentration before lyophilization ~0.8mg/ml (lot dependent, please refer to CoA along with shipment for actual concentration). Buffer before lyophilization: Phosphate buffered saline (PBS), pH 7.4, 1% BSA, 0.025% NaN3.
• Purification: Affinity purified on immobilized antigen.
• Conjugation: Unconjugated
• Storage: Store at -20°C as received.
• Stability: Stable for 12 months from date of receipt.
• Gene Name: solute carrier family 1 (glial high affinity glutamate transporter), member 2
• Database Link:
  NP_058911
  Entrez Gene 6506 HumanEntrez Gene 20511 MouseEntrez Gene 29482 Rat
  UniProt ID P31596
• Background: L-Glutamate (Glu) is an abundant amino acid that functions as the major excitatory neurotransmitter in the central nervous system. However, excess of Glu in the extracellular synaptic milieu leads to neuronal cell death by a process known as excitotoxicity. The extracellular levels of Glu are regulated by a family of high affinity plasma membrane transporters called excitatory amino acid transporters (EAATs) which are responsible for the re-uptake of Glu into the cells. The EAAT family includes five members (EAAT1-EAAT5) that are members of the solute carrier family 1 (SLC1) of Na+-dependent transporters that also includes the neutral amino acid transporters ASCT1 and ASCT2. The Glu transporters present an unusual topology of eight transmembrane domains with two re-entrant loops and intracellular N- and C- termini. The transporter is likely assembled as a trimer where each monomer is a functional unit capable of binding the Glu substrate. The transport of Glu into the cells by the EAAT transporters is coupled to the Na+ and K+ electrochemical gradient as a driving force. Hence, the uptake of Glu is dependent on the co-transport of three Na+ and one H+ ions, and the counter transport of one K+ ion. In addition, to the well documented Glu uptake, the EAAT transporters show a Glu-independent Cl conductance. The physiological significance of the Cl current through the EAATs is currently unknown. EAAT2 (also known as Glutamate Transporter-1, GLT-1) as well as EAAT1, is expressed predominantly in glia cells, while EAAT3, EAAT4 and EAAT5 are mostly expressed in neurons. As mentioned earlier, EAAT transporters represent the only (significant) mechanism for removal of glutamate from the extracellular fluid and hence are essential for the long-term maintenance of low and non-toxic concentrations of glutamate and the preservation of normal excitatory synaptic transmission. In addition to Glu uptake, the glutamate transporters provide glutamate for the synthesis of g-Aminobutyric acid (GABA), glutathione and protein, suggesting an interactive role between EAATs and cellular metabolism. Dysregulation of EAAT activities has been implicated in several neurodegenerative disorders such as Alzheimerâ??s disease, traumatic brain injury, epilepsy and schizophrenia, suggesting that EAATs can be a useful target for the treatment of these conditions.
• Synonyms: EAAT2; GLT-1; GLT1