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Glutamate transporter EAAC

TTie actual meanings of the acronyms (GLAST, glutamate-aspartate transporter GLT. glutamate transporter EAAC. excitatory amino acid carrier EAAT. excitatory amino acid transporter) are not important, as they do not reflect functional differences among the transporters. [Pg.232]

Peghini P, Janzen J, Stoffel W (1997) Glutamate transporter EAAC-1-deficient mice develop dicarboxylic aminoaciduria and behavioral abnormalities but no neurodegeneration. EMBO J 76 3822-3832. [Pg.251]

Although significant progress has been made in recent years, essential pieces of information are still lacking. This includes information on the amount of glutamate released (see below) and on the densities of EAAC and the nerve terminal glutamate transporter. [Pg.243]

EAAC rabbit glutamate transporter (Kanai and Hediger, 1992)... [Pg.246]

Glutamate and sodium/lithium-induced conformational changes in the GLT-1 transporter have been detected by the altered accessibility of trypsin-sensitive sites to the protease (59). These experiments in GLT-1 shows that lithium can occupy at least one of the sodium ion binding sites, but lithium by itself cannot support coupled transport (59). Therefore, at least one of the sodium binding sites in GLT-1 discriminates between sodium and lithium. As described earlier, this contrasts with EAAC-1, where lithium is able to support uptake. It should therefore be possible to identify residues that are responsible for the sodium/lithium selectivity difference between EAAC-1 and GLT-1. [Pg.155]


See other pages where Glutamate transporter EAAC is mentioned: [Pg.147]    [Pg.148]    [Pg.232]    [Pg.233]    [Pg.234]    [Pg.242]    [Pg.243]    [Pg.245]    [Pg.151]    [Pg.155]    [Pg.411]    [Pg.234]    [Pg.242]   
See also in sourсe #XX -- [ Pg.302 ]




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Glutamate transport

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