Solute carrier family 38, member 1/sodium-coupled neutral amino acid transporter 1 (SLC38A1, ATA1, NAT2, SAT1, SNAT1), which is expressed during embryogenesis, is a sodium-dependent transporter of neutral zwitterionic amino acids, such a glutamine. SLC38A1/SAT1 is believed to be involved in translocation of glutamine into GABAergic neurons to facilitate inhibitory neurotransmitter generation.
Specificity
Anti-SLC38A1 (AB1) polyclonal antibody reacts with canine and human solute carrier family 38, member 1 proteins.
Immunogen
Synthetic peptide directed towards the middle region of human SLC38A1
Application
Anti-SLC38A1 (AB1) polyclonal antibody is used to tag solute carrier family 38, member 1/sodium-coupled neutral amino acid transporter for detection and quantitation by Western blotting and in plasma by immunohistochemical (IHC) techniques. It is used as a probe to determine the roles of solute carrier family 38, member 1 in transport of important neutral zwitterionic amino acids, such a glutamine, during embryogenesis and in neural function.
Biochem/physiol Actions
Amino acid transporters play essential roles in the uptake of nutrients, production of energy, chemical metabolism, detoxification, and neurotransmitter cycling. SLC38A1 is an important transporter of glutamine, an intermediate in the detoxification of ammonia and the production of urea. Glutamine serves as a precursor for the synaptic transmitter, glutamate.
Sequence
Synthetic peptide located within the following region: LLKNLGYLGYTSGFSLSCMVFFLIVVIYKKFQIPCIVPELNSTISANSTN
Physical form
Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Journal of molecular endocrinology, 63(4), 239-248 (2019-09-11)
Excess maternal glucocorticoids reduce placental amino acid transport and fetal growth, but whether these effects are mediated directly on the syncytiotrophoblast remains unknown. We hypothesised that glucocorticoids inhibit mechanistic target of rapamycin (mTOR) signaling and insulin-stimulated System A amino acid
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