GAT1 (E7J1B) Rabbit mAb (Alexa Fluor® 488 Conjugate) #18446
- IF
Supporting Data
| REACTIVITY | H M R |
| SENSITIVITY | Endogenous |
| MW (kDa) | |
| Source/Isotype | Rabbit IgG |
Application Key:
- IF-Immunofluorescence
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
Product Information
Product Description
Product Usage Information
| Application | Dilution |
|---|---|
| Immunofluorescence (Frozen) | 1:50 |
Storage
Protocol
Specificity / Sensitivity
GAT1 (E7J1B) Rabbit mAb (Alexa Fluor® 488 Conjugate) 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).
- Kristensen, A.S. et al. (2011) Pharmacol Rev 63, 585-640.
- Borden, L.A. (1996) Neurochem Int 29, 335-56.
- Moldavan, M. et al. (2017) J Neurophysiol 118, 3092-106.
- Lorenz-Guertin, J.M. and Jacob, T.C. (2018) Dev Neurobiol 78, 238-70.
- Skovstrup, S. et al. (2010) ChemMedChem 5, 986-1000.
- Bragina, L. et al. (2008) J Neurochem 105, 1781-93.
- Jensen, K. et al. (2003) J Neurophysiol 90, 2690-701.
- Liu, G.X. et al. (2007) Neuropsychopharmacology 32, 1531-9.
- Xu, Y.F. et al. (2008) J Neurosci Res 86, 465-70.
- Whitworth, T.L. and Quick, M.W. (2001) J Biol Chem 276, 42932-7.
- Law, R.M. et al. (2000) J Biol Chem 275, 23986-91.
- Giros, B. et al. (1996) Nature 379, 606-12.
- Chen, N. et al. (2004) J Biol Chem 279, 5508-19.
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