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Details for receptor: GLAST

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  • General information
  • Subunits
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EndoNet ID: ENR01221

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Synonyms

  • GLAST
  • GLAST-1
  • GLAST1
  • excitatory amino acid transporter 1
  • SLC1A3
  • solute carrier family 1 member 3
  • sodium-dependent glutamate/aspartate transporter 1
  • EAAT1

General information

  • The glutamate transporters in the plasma membranes of neural cells secure termination of the glutamatergic synaptic transmission and keep the glutamate levels below toxic concentrations. [1]
  • Transports L-glutamate and also L- and D-aspartate, essential for terminating the postsynaptic action of glutamate by rapidly removing released glutamate from the synaptic cleft. [2]
  • Defects in SLC1A3 are the cause of episodic ataxia type 6 (EA6). [2]

Links to other resources

UniProt P43003
Ensembl ENST00000427100

Subunit information

Sequence 
MTKSNGEEP KMGGRMERF QQGVRKRTL 
LAKKKVQNI TKEDVKSYL FRNAFVLLT 
VTAVIVGTI LGFTLRPYR MSYREVKYF 
SFPGELLMR MLQMLVLPL IISSLVTGM 
AALDSKASG KMGMRAVVY YMTTTIIAV 
VIGIIIVII IHPGKGTKE NMHREGKIV 
RVTAADAFL DLIRNMFPP NLVEACFKQ 
FKTNYEKRS FKVPIQANE TLVGAVINN 
VSEAMETLT RITEELVPV PGSVNGVNA 
LGLVVFSMC FGFVIGNMK EQGQALREF 
FDSLNEAIM RLVAVIMWY APVGILFLI 
AGKIVEMED MGVIGGQLA MYTVTVIVG 
LLIHAVIVL PLLYFLVTR KNPWVFIGG 
LLQALITAL GTSSSSATL PITFKCLEE 
NNGVDKRVT RFVLPVGAT INMDGTALY 
EALAAIFIA QVNNFELNF GQIITISIT 
ATAASIGAA GIPQAGLVT MVIVLTSVG 
LPTDDITLI IAVDWFLDR LRTTTNVLG 
DSLGAGIVE HLSRHELKN RDVEMGNSV 
IEENEMKKP YQLIAQDNE TEKPIDSET 
KM

Binding hormones

  • L-glutamate
    • Three glutamate transporters expressed in human motor cortex, termed EAAT1 , EAAT2, and EAAT3. [3]
  • L-aspartate
  • D-aspartate

Anatomical structures with this receptor

  • astrocyte

    Induced phenotypes

    • excitotoxcicity
      • The glutamate receptor GLAST maintains low synaptic glutamate levels to terminate glutamate signaling and prevent pathologic excitotoxicity. [4]

  • bergmann_glia

    Induced phenotypes

    • neuronal hyperexcitability
      • Heterozygous mutation in GLAST leads to neuronal hyperexcitability that causes seizures, hemiplegia and episodic ataxia. [5]
    • termination of excitatory nerve signals
      • GLAST regulates the uptake of glutamate, important for the termination of excitatory signals and the maintenance of non-toxic concentrations. [6]

  • oligodendrocyte

    Induced phenotypes

    • excitotoxcicity
      • The uptake of glutamate from the synaptic cleft by GLAST is crucial for the termination of excitatory neurotransmission. thereby preventing pathologic excitotoxicity. [7]
Reference