SLC1A1 antibody

Background of SLC1A1 antibody

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 syptic milieu leads to neurol 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 +-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 functiol unit capable of binding the Glu substrate. The transport of Glu into the cells by the EAAT transporters is coupled to the + and K+ electrochemical gradient as a driving force. Hence, the uptake of Glu is dependent on the co-transport of three + 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 as well as EAAT1 are expressed predomintly in glia cells, while EAAT3 (Excitatory Amino Acid Transporter 3), EAAT4 and EAAT5 are mostly expressed in neurons. As mentioned, EAAT transporters represent the only (significant) mechanism for removal of glutamate from the extracellular fluid and hence are essential for the long-term maintence of low and non-toxic concentrations of glutamate and the preservation of normal excitatory syptic 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.