GAT3 Antibody #25438
Filter:
- WB
Supporting Data
REACTIVITY | H M R |
SENSITIVITY | Endogenous |
MW (kDa) | 70, 140 |
SOURCE | Rabbit |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
Product Information
Product Usage Information
Application | Dilution |
---|---|
Western Blotting | 1:1000 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
GAT3 Antibody recognizes endogenous levels of total GAT3 protein.
Species Reactivity:
Human, Mouse, Rat
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro604 of human GAT3 protein. Antibodies are purified by peptide affinity chromatography.
Background
The solute carrier 6 (SLC6) gene, also known as the neurotransmitter–sodium-symporter family or Na+/Cl- -dependent transporters, encodes for proteins that regulate neurotransmitter (NTT) transport, including monoamine transmitters serotonin, dopamine, and norepinephrine (SERT), GABA transmitters (GAT1, GAT2, GAT3, and BGT1), and glycine transmitters (GLYT1 and GLYT2) (1). The sodium- and chloride-dependent GABA transporter 3 (GAT3) is encoded by the solute carrier family 6 member 11 (SLC6A11) gene (2). GABA is the principal inhibitory neurotransmitter in the central nervous system and maintains the inhibitory tone that balances out neuronal excitation. This balance between neuronal excitation and inhibition is tightly regulated, in part by the GAT family of GABA transporters. These transporters terminate GABA inhibition by mediating cellular reuptake of GABA at the synaptic cleft. The human genome encodes four GABA transports (GAT-1-4). GAT-1 is found predominantly in the axon terminals of neurons whereas GAT-3 is expressed in astrocytes (3). Dysfunction of GABA transporters may contribute to diseases such as epilepsy as well as neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease (4-6).
- Kristensen, A.S. et al. (2011) Pharmacol Rev 63, 585-640.
- Soudijn, W. and van Wijngaarden, I. (2000) Curr Med Chem 7, 1063-79.
- Jin, X.T. et al. (2011) Front Syst Neurosci 5, 63.
- Sałat, K. and Kulig, K. (2011) Future Med Chem 3, 211-22.
- Chazalon, M. et al. (2018) Cell Rep 23, 1678-90.
- Fuhrer, T.E. et al. (2017) Neuroscience 351, 108-18.
限制使用
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For Research Use Only. Not For Use In Diagnostic Procedures.
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