Render Target: STATIC
Render Timestamp: 2024-10-11T09:56:56.282Z
Commit: 56767fe525c928647c8401233a175d0d607d385d
XML generation date: 2024-09-30 01:57:47.133
Product last modified at: 2024-09-30T08:02:10.162Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

GAT1 (E7J1B) Rabbit mAb #37342

Filter:
  • WB
  • IP
  • IF

    Supporting Data

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa) 65
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • IF-Immunofluorescence 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:100
    Immunofluorescence (Frozen) 1:100 - 1:200

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    GAT1 (E7J1B) Rabbit mAb recognizes endogenous levels of total GAT1 protein.

    Species Reactivity:

    Human, Mouse, Rat

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human GAT1 protein.

    Background

    The solute carrier 6 gene (SLC6), also known as the neurotransmitter–sodium-symporter family or Na+/Cl- -dependent transporter, encodes for proteins that regulate neurotransmitter (NTT) transport, including monoamine transmitters serotonin, dopamine, and norepinephrin (SERT), GABA transmitters (GAT1, GAT2, GAT3, and BGT1), and glycine transmitters (GLYT1 and GLYT2) (1). These proteins express ubiquitously in the brain and regulate the release and uptake of neurotransmitters in terminal clefts, in both neuronal and non-neuronal cells (2-4). Dysregulation of NTT-transporters is associated with neurological disease like epilepsy, schizophrenia, anxiety, bipolar disorder, and addictions to cocaine and methamphetamines (1). Inhibitors of NTT-transporters are widely used as drugs to treat disorders like depression (tricyclic antidepressants), and antiepileptic tiagabine (5). GAT1 is the only GABA transporter genetically studied in GAT1-KO mouse models where an accumulation of extracellular GABA decreased anxiety and depression-like behaviors (6-8). The lack or reduction of GAT1 diminished aggression in mice, and a condition known as hypoalgesia, where there is a decreased sensitivity to painful stimuli (8,9). GAT1 posttranslational modifications include phosphorylation at Tyr107 (IL1), and Tyr317 (IL3), and these mutations identify as the phospho-acceptor-sites, therefore regulating GAT1 (10,11). GABA trafficking is regulated by Tyr phosphorylation, and it has been shown that activation of adenosine A2A receptors in the hippocampus synaptosomes enhanced BAGA uptake by opposing a constitutive PKC-mediated downregulation of GAT1 (11-13).
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