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Showing SLC1A1 — EAAC1 is a alias.

SLC1A1

Excitatory amino acid transporter 3 · UniProt P43005

Length
524 aa
Mass
57.1 kDa
Annotated
2026-06-10
100 papers in source corpus 34 papers cited in narrative 34 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/7 claims corpus-supported (86%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SLC1A1 (EAAC1/EAAT3) is a Na+-dependent, high-affinity plasma membrane transporter for glutamate, aspartate, and cysteine whose activity is governed largely by rapid, regulated trafficking between an intracellular pool and the cell surface, where the protein has a half-life of only ~5–7 minutes due to constitutive recycling (PMID:15197183). Surface delivery and transport are acutely stimulated through parallel signaling routes: PKC activation increases transport, with PKCα forming direct EAAC1–PKCα complexes that drive surface expression while PKCε raises intrinsic activity (PMID:8764574, PMID:12843260, PMID:12237337), and PDGF acts through PI3K→Akt to redistribute the transporter to the membrane (PMID:10671571, PMID:16182322); both regulated pathways depend on a C-terminal (502)YVN(504) motif (PMID:16368696). ER exit and surface stability are set by competing interactions at the cytoplasmic tail—GTRAP3-18 binds the C-terminus to lower substrate affinity and restrain ER export, while RTN2B and ARL6IP1 oppose GTRAP3-18 to promote forward trafficking (PMID:11242046, PMID:18096700, PMID:18684713), and the sorting receptor SorCS2 sustains surface levels (PMID:30840898); conversely syntaxin 1A drives clathrin-mediated endocytosis and degradation (PMID:16959903). Functionally, EAAC1 imports cysteine to support neuronal glutathione synthesis and antioxidant/zinc-buffering defense, such that its loss exacerbates ischemic and epileptic neuronal death (PMID:20357106, PMID:21084597, PMID:17646425, PMID:30840898), and the same glutamate-recycling/cysteine-supply logic drives glutathione biosynthesis and survival in cancer cells via cooperation with system Xc- (PMID:33229341). Independent of transport, the EAAC1 N-terminus binds holocytochrome c synthetase to preserve XIAP activity and confer an anti-apoptotic function (PMID:16858406). In vivo, EAAC1 controls midbrain presynaptic dopaminergic signaling and OCD-like behaviors (PMID:28507136, PMID:30622300), and loss-of-function mutations cause human dicarboxylic aminoaciduria, establishing it as the major renal acidic-amino-acid transporter (PMID:21123949, PMID:9435692). A distinct vascular role imports the oncometabolite R-2-hydroxyglutarate into endothelial mitochondria to drive Na+/Ca2+ exchange and tumor angiogenesis (PMID:35459936).

Mechanistic history

Synthesis pass · year-by-year structured walk · 20 steps
  1. 1996 High

    Established that EAAC1 transport is acutely regulated by intracellular signaling rather than only by expression level, opening the question of how a kinase changes transporter output.

    Evidence PKC activation by phorbol ester in C6 glioma, with kinetic analysis and PKC inhibitors

    PMID:8764574

    Open questions at the time
    • Did not determine whether increased Vmax reflected more surface transporters or higher per-molecule activity
    • PKC isoform not identified
  2. 2000 High

    Showed the regulatory mechanism is trafficking-based, linking growth-factor signaling to physical redistribution of the transporter to the membrane.

    Evidence PDGF stimulation with surface biotinylation, PI3K activity assay, and PI3K inhibitors

    PMID:10671571

    Open questions at the time
    • Downstream effector of PI3K not yet defined
    • Trafficking step (delivery vs. retrieval) not resolved
  3. 2001 High

    Identified a direct C-terminal binding partner (GTRAP3-18) that suppresses transport by lowering substrate affinity, defining a protein-interaction mode of regulation distinct from trafficking.

    Evidence Co-IP, C-terminal domain mapping, and glutamate uptake assays with retinoic-acid induction

    PMID:11242046

    Open questions at the time
    • Mechanism by which affinity is lowered not structurally resolved
    • Whether GTRAP3-18 acts in ER vs. plasma membrane not yet distinguished
  4. 2001 Medium

    Revealed cell-type specificity of PKC regulation, showing the same kinase can drive opposite trafficking outcomes.

    Evidence Xenopus oocyte electrophysiology, capacitance measurement, and PKC inhibitors

    PMID:11578612

    Open questions at the time
    • Molecular basis for opposite directionality between oocytes and glioma not resolved
    • Single expression system
  5. 2002 High

    Defined PKCα vs. PKCε division of labor (surface expression vs. intrinsic activity) and added a Gq-coupled receptor, cytoskeleton-dependent route, broadening the regulatory network.

    Evidence PKC subtype-selective inhibition/downregulation with biotinylation; NTS1-driven aspartate uptake with cytoskeletal disruptors

    PMID:12123836 PMID:12237337

    Open questions at the time
    • Substrate(s) phosphorylated by each PKC isoform unknown
    • How NTS1 couples to cytoskeleton-dependent insertion unresolved
  6. 2003 High

    Demonstrated PKCα physically complexes with EAAC1, providing a molecular basis for isoform-specific surface regulation in cells and native brain tissue.

    Evidence Reciprocal co-IP in C6 glioma and synaptosomes plus confocal colocalization

    PMID:12843260

    Open questions at the time
    • Direct vs. adaptor-mediated contact not established
    • Phosphorylation site(s) on EAAC1 not mapped
  7. 2004 High

    Quantified the rapid constitutive recycling of EAAC1 and separated basal from regulated intracellular pools, clarifying which trafficking step each stimulus controls.

    Evidence Multiple biotinylation/internalization strategies and temperature-block experiments in two cell systems

    PMID:15197183

    Open questions at the time
    • Identity of the regulated intracellular compartment not defined
    • SNARE/vesicle machinery not yet identified
  8. 2004 Medium

    Placed SGK1 (and PKB) as kinases stimulating EAAT3 transport, extending the kinase regulatory network.

    Evidence Xenopus oocyte voltage clamp with active/inactive SGK1 and PKB constructs plus retinal colocalization

    PMID:15111600

    Open questions at the time
    • Direct vs. indirect kinase action not established
    • Trafficking step affected not resolved
  9. 2005 High

    Identified the cytoplasmic effector and the precise C-terminal motif required for regulated trafficking, and showed homotrimer subunits transport independently.

    Evidence Akt dominant-negative/constitutively-active rescue; EAAC1/GLT-1 chimeras and YVN alanine scanning; coexpression electrophysiology of WT and affinity mutants

    PMID:16128593 PMID:16182322 PMID:16368696

    Open questions at the time
    • Whether YVN is directly phosphorylated or serves as a binding site unknown
    • How independent subunit gating relates to regulated trafficking not addressed
  10. 2006 Medium

    Resolved the endocytic and exocytic SNARE machinery, showing syntaxin 1A promotes clathrin-mediated removal/degradation while SNAP-23 SNAREs drive constitutive delivery.

    Evidence Syntaxin 1A domain deletions with siRNA knockdown and endocytosis/degradation assays; SNARE profiling with dominant-negative SNAP-23 and rate-of-delivery assays

    PMID:16516346 PMID:16959903

    Open questions at the time
    • Whether syntaxin 1A binds EAAC1 directly not fully established
    • Cell-type variation in SNARE usage not reconciled
  11. 2006 High

    Uncovered a transport-independent anti-apoptotic function: the EAAC1 N-terminus sequesters HCCS to preserve XIAP and block caspase-3.

    Evidence N-terminal co-IP with HCCS, HCCS–XIAP competition binding, caspase-3 assays, and PC12/motor neuron rescue

    PMID:16858406

    Open questions at the time
    • Structural basis of N-terminal HCCS binding not defined
    • In vivo contribution relative to glutathione function unclear
  12. 2007 High

    Defined the positive trafficking arm at the ER and at the membrane, with RTN2B promoting ER exit by counteracting GTRAP3-18 and surface GTRAP3-18 controlling cysteine uptake/glutathione.

    Evidence RTN2B co-IP, domain mapping, surface expression and neuronal siRNA; GTRAP3-18 gain/loss with GSH and oxidative-stress readouts

    PMID:17646425 PMID:18096700

    Open questions at the time
    • Quantitative balance between GTRAP3-18 and RTN2B at steady state unknown
    • How retinoic acid couples to oxidative-stress state not detailed
  13. 2008 Medium

    Showed ARL6IP1 tunes transport indirectly by competing for GTRAP3-18, adding a regulator-of-regulator layer that raises substrate affinity.

    Evidence Co-IP, addicsin hydrophobic-region mutagenesis, and kinetic transport assays under PKC activation

    PMID:18684713

    Open questions at the time
    • In vivo relevance not tested
    • Single lab, single system
  14. 2010 High

    Connected EAAC1 trafficking and cysteine supply to disease and stress, showing recycling-endosome defects, knockout, and ischemia converge on glutathione/zinc dysregulation and neuronal death.

    Evidence Rab11 dominant-active rescue in HD knock-in neurons; EAAC1-/- mice in cerebral ischemia with NAC rescue, zinc and superoxide readouts

    PMID:20357106 PMID:21084597

    Open questions at the time
    • Relative contribution of cysteine supply vs. glutamate clearance to neuroprotection not separated
    • Recycling-endosome adaptor for EAAC1 not identified
  15. 2010 High

    Established SLC1A1 as the major human renal acidic amino-acid transporter through loss-of-function mutations causing dicarboxylic aminoaciduria, and added AMPK and PIP5K2A as regulators.

    Evidence Patient mutations R445W/I395del with transport and surface assays in kidney cells; Xenopus/HEK electrophysiology and surface assays for AMPK and PIP5K2A

    PMID:19644675 PMID:20218975 PMID:21123949

    Open questions at the time
    • Renal vs. neuronal disease mechanisms not unified
    • Direct vs. indirect action of AMPK/PIP5K2A on EAAT3 unresolved
  16. 2012 Medium

    Added mTOR as a delivery-promoting regulator and described a mitochondrial EAAC1–NCX1 partnership supporting glutamate-stimulated ATP synthesis.

    Evidence Xenopus mTOR coexpression with rapamycin/brefeldin A; mitochondrial localization imaging, EAAC1–NCX1 co-IP, and antisense ATP assays

    PMID:22479505 PMID:22483750

    Open questions at the time
    • How a plasma-membrane transporter reaches mitochondria not explained
    • mTOR effect mechanism (direct vs. via Akt/SGK) unresolved
  17. 2013 Medium

    Showed alternative SLC1A1 isoforms act as dominant inhibitors of the full-length transporter, adding transcript-level regulation relevant to psychiatric phenotypes.

    Evidence Isoform cloning, co-IP/colocalization, and glutamate-uptake inhibition assays

    PMID:23695234

    Open questions at the time
    • Mechanism of dominant-negative inhibition not mapped
    • Physiological abundance of isoforms unknown
  18. 2018 High

    Linked EAAT3 dosage to behavior and synaptic physiology in vivo, with midbrain loss reducing striatal dopamine and overexpression producing OCD-like, fluoxetine-reversible phenotypes.

    Evidence STOP-cassette conditional KO with regional viral rescue and microdialysis; CaMKIIα-driven overexpression with behavior, corticostriatal electrophysiology, and drug rescue

    PMID:28507136 PMID:30622300

    Open questions at the time
    • Molecular link between transport activity and dopamine release not defined
    • Whether glutamate clearance or cysteine supply drives behavior unresolved
  19. 2019 High

    Identified SorCS2 as a sorting receptor sustaining EAAT3 surface levels for cysteine import, with deficiency causing oxidative damage and worse epilepsy outcomes.

    Evidence SorCS2-knockout mice with surface expression, cysteine uptake, GSH, and neuronal death assays in epilepsy

    PMID:30840898

    Open questions at the time
    • Trafficking itinerary controlled by SorCS2 not mapped
    • Relationship to GTRAP3-18/RTN2B network unexamined
  20. 2022 High

    Extended SLC1A1 beyond neurons and amino acids, showing endothelial import of the oncometabolite R-2-HG to mitochondria drives Na+/Ca2+ exchange and tumor angiogenesis; and that glutamate recycling fuels cancer glutathione synthesis via system Xc-.

    Evidence SLC1A1-KO mice and endothelial assays with R-2-HG uptake/fractionation and mitochondrial respiration; isotope-tracing metabolomics in lung cancer with knockdown/overexpression

    PMID:33229341 PMID:35459936

    Open questions at the time
    • Substrate selectivity allowing R-2-HG transport not structurally defined
    • Whether mitochondrial localization seen in neurons applies to endothelial cells unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the multiple converging regulators (PKC isoforms, PI3K/Akt, SGK1, mTOR, AMPK, GTRAP3-18/RTN2B/ARL6IP1, syntaxin 1A, SNAP-23, SorCS2) are integrated on a single C-terminal/N-terminal interface to set net surface density in a given cell type remains unresolved.
  • No unified structural model of the regulated cytoplasmic interface
  • Hierarchy and crosstalk among kinase and adaptor pathways not established
  • Tissue-specific determinants of opposite PKC outcomes unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005215 transporter activity 7 GO:0140313 molecular sequestering activity 1
Localization
GO:0005886 plasma membrane 4 GO:0005739 mitochondrion 2 GO:0005768 endosome 1 GO:0005783 endoplasmic reticulum 1
Pathway
R-HSA-382551 Transport of small molecules 4 R-HSA-9609507 Protein localization 4 R-HSA-112316 Neuronal System 3 R-HSA-8953897 Cellular responses to stimuli 2 R-HSA-5357801 Programmed Cell Death 1
Partners
ARL6IP1GTRAP3-18HCCSNCX1PRKCARTN2BSORCS2STX1A

Evidence

Reading pass · 34 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 GTRAP3-18 specifically interacts with the carboxy-terminal intracellular domain of EAAC1/SLC1A1; overexpression of GTRAP3-18 reduces EAAC1-mediated glutamate transport by lowering substrate affinity without affecting total transporter expression. GTRAP3-18 expression can be upregulated by retinoic acid, producing a specific reduction in EAAC1-mediated transport. Co-immunoprecipitation, pulldown mapping of C-terminal domain interaction, glutamate uptake assays in cells with overexpressed GTRAP3-18, retinoic acid treatment Nature High 11242046
1996 Activation of protein kinase C (PKC) by phorbol ester (PMA) rapidly increases EAAC1-mediated glutamate transport activity in C6 glioma cells via a 2.5-fold increase in Vmax with no change in Km, independent of protein synthesis. An inactive phorbol ester and the PKC inhibitor chelerythrine block this effect. Radiolabeled glutamate uptake assays, kinetic analysis, pharmacological inhibitors (chelerythrine, cycloheximide), inactive phorbol ester controls Journal of neurochemistry High 8764574
2000 Platelet-derived growth factor (PDGF) rapidly increases EAAC1 activity and cell surface expression via activation of phosphatidylinositol 3-kinase (PI3K). PDGF causes redistribution of EAAC1 from an intracellular compartment to the plasma membrane; this effect is blocked by PI3K inhibitors wortmannin and LY294002 but not by a PKC inhibitor. Membrane-impermeant biotinylation combined with Western blotting to measure surface EAAC1, radiolabeled glutamate uptake, PI3K activity assay, pharmacological inhibitors The Journal of biological chemistry High 10671571
2003 PKC activation with PMA induces formation of EAAC1-PKCα complexes but not EAAC1-PKCδ complexes in C6 glioma cells, and causes EAAC1 and PKCα to colocalize in clusters at or near the cell surface. EAAC1-PKCα complexes are also detected in rat brain synaptosomes. This interaction is blocked by PKC inhibitors. Co-immunoprecipitation in C6 glioma and synaptosomes, confocal microscopy colocalization, pharmacological inhibitors The Journal of neuroscience High 12843260
2002 PKCα mediates the PKC-dependent increase in EAAC1 cell surface expression, while PKCε mediates an increase in EAAC1 transport activity independent of changes in surface expression (increased Vmax without surface redistribution). Gö6976 (PKCα inhibitor) completely blocks surface expression increase but only partially attenuates activity increase; PKC subtype-selective downregulation confirms this dissociation. PKC subtype identification by Western blot, selective inhibitor Gö6976, PKC downregulation by prolonged phorbol ester treatment, biotinylation assay, uptake assays Molecular pharmacology High 12237337
2004 EAAC1 has a half-life of approximately 5–7 min at the plasma membrane due to rapid constitutive recycling. Both PKC (phorbol ester) and PDGF accelerate delivery of EAAC1 to the cell surface; PKC additionally inhibits endocytosis of EAAC1, whereas PDGF does not. Basal and regulated pools of EAAC1 exist in distinct intracellular compartments, as incubation at 18°C blocks regulated but not basal trafficking. Multiple biotinylation strategies (surface labeling at 37°C, reversible biotinylation to measure internalization), temperature block experiments in C6 glioma and primary neuronal cultures The Journal of biological chemistry High 15197183
2005 A carboxyl-terminal motif (502)YVN(504) in EAAC1 is required for both PDGF-dependent and PKC-dependent regulated trafficking to the cell surface. A 12-amino acid sequence starting at this tyrosine is sufficient to confer PDGF-responsiveness to a non-responsive chimera. The glial transporter GLT-1 carboxyl terminus does not confer regulated trafficking, but replacing it with EAAC1's carboxyl terminus does. Domain chimeras between EAAC1 and GLT-1, alanine substitution mutagenesis, truncation mutants, biotinylation surface expression assays in C6 glioma The Journal of biological chemistry High 16368696
2005 Akt (PKB) is required downstream of PI3K for PDGF-induced redistribution and increased surface expression of EAAC1. A dominant-negative Akt-1 blocks PDGF-induced EAAC1 redistribution; constitutively active Akt-1 increases EAAC1 surface expression; lentiviral CA-Akt-1 increases both surface EAAC1 and Na+-dependent glutamate transport activity. Dominant-negative and constitutively active Akt-1 transfection, lentiviral expression of CA-Akt, biotinylation surface expression assay, glutamate uptake assay, Akt phosphorylation (Ser473) measurement Neuropharmacology High 16182322
2005 Individual subunits within the EAAC1 homotrimer function independently of each other. Coexpression of EAAC1(WT) with EAAC1(R446Q) (transports glutamine not glutamate) produces purely additive anion currents. Coexpression with EAAC1(H295K) (90-fold reduced glutamate affinity) yields two independent populations matching individual subunit affinities. pH-dependence studies with EAAC1(E373Q) similarly show independent subunit function. Electrophysiology (anion currents), coexpression of WT and mutant subunits in cells, glutamate concentration-response curves, pH-dependence assays Biochemistry High 16128593
2007 RTN2B, a reticulon protein localized in the ER and ER exit sites, interacts with EAAC1 and with GTRAP3-18, binding to different regions of RTN2B. RTN2B enhances ER exit and cell surface expression of EAAC1 in heterologous cells. siRNA knockdown of RTN2B decreases EAAC1 protein levels in neurons. Thus RTN2B acts as a positive regulator of EAAC1 trafficking from ER to cell surface, counteracting GTRAP3-18. Co-immunoprecipitation of RTN2B with EAAC1 and GTRAP3-18, domain binding analysis, surface expression assays in heterologous cells, siRNA knockdown in neurons, Western blotting The Journal of biological chemistry High 18096700
2006 Syntaxin 1A promotes endocytic sorting of EAAC1 via clathrin-mediated internalization, leading to functional inhibition of glutamate transport. The H3 coiled-coil domain of syntaxin 1A (in the presence of its transmembrane domain) is necessary and sufficient for this inhibitory effect. Endogenous syntaxin 1A knockdown blocks EAAC1 endocytic sorting and lysosomal degradation triggered by kainic acid. Clathrin-mediated endocytosis assays, syntaxin 1A domain deletion constructs, co-immunoprecipitation, siRNA knockdown in rat model, glutamate transport functional assay Journal of cell science High 16959903
2006 A dominant-negative variant of SNAP-23 (lacking the SNARE domain) decreases EAAC1 surface expression and slows constitutive delivery of EAAC1 to the plasma membrane. C6 glioma expresses syntaxin 4, VAMP2, and SNAP-23 but not syntaxin 1A, VAMP1, or SNAP-25, indicating that SNAP-23-containing SNARE complexes (not syntaxin 1A) are required for constitutive EAAC1 recycling. Western blotting of SNARE proteins, co-transfection with dominant-negative SNAP-23, biotinylation surface expression assay, rate-of-delivery assay, Myc-tagged EAAC1 Neurochemistry international Medium 16516346
2002 Activation of the Gq/11-coupled neurotensin receptor NTS1 rapidly increases EAAC1-mediated aspartate uptake (~70%) in C6 glioma by increasing cell surface expression of EAAC1 via a cytoskeleton-dependent mechanism. Cytochalasin D and colchicine (actin and microtubule disruptors) block this effect, whereas PKC and PI3K inhibitors do not. Radiolabeled D-aspartate uptake assay, stable NTS1-expressing C6 glioma, cytoskeletal inhibitors (cytochalasin D, colchicine), PKC and PI3K inhibitor controls FEBS letters Medium 12123836
2010 In Huntington's disease knock-in neurons, mutant huntingtin causes defective Rab11-dependent recycling endosome trafficking, leading to reduced cell surface levels of EAAC1 and impaired cysteine uptake. Expression of dominant-active Rab11 in HD neurons restores EAAC1 surface expression, cysteine uptake, intracellular glutathione, ROS clearance, and neuronal survival. Cell surface biotinylation, cysteine uptake assays, glutathione measurement, ROS assays, dominant-active Rab11 rescue in primary HD neurons from HD140Q/140Q knock-in mice The Journal of neuroscience High 20357106
2010 Loss of EAAC1 (EAAC1-/- mice) impairs neuronal cysteine uptake, reduces glutathione synthesis, increases cytosolic and vesicular zinc, and exacerbates hippocampal neuronal death after transient cerebral ischemia (~2-fold). N-acetylcysteine treatment restores glutathione, normalizes zinc levels, and reduces ischemia-induced zinc translocation, superoxide production, and neuronal death. EAAC1 knockout mouse model, transient cerebral ischemia model, histological neuronal death quantification, zinc fluorescence, superoxide detection, NAC pharmacological rescue The Journal of neuroscience High 21084597
2010 Loss-of-function mutations R445W and I395del in SLC1A1 impede or abolish glutamate and cysteine transport, and lead to near-absent surface expression in a kidney cell line, causing human dicarboxylic aminoaciduria. This establishes SLC1A1 as the major renal transporter of glutamate and aspartate in humans. Transport assays in kidney cell line expressing mutant SLC1A1, surface expression assays, identification of R445W and I395del mutations in human patients with dicarboxylic aminoaciduria The Journal of clinical investigation High 21123949
2004 SGK1 (serum- and glucocorticoid-inducible kinase 1) co-localizes with EAAT3 in retinal ganglion cells and stimulates EAAT3-mediated glutamate transport when co-expressed in Xenopus oocytes. Constitutively active SGK1 (S422D) and constitutively active PKB stimulate transport, whereas inactive SGK1 (K127N) does not. Immunohistochemistry for colocalization, Xenopus oocyte expression with dual electrode voltage clamp, constitutively active and dominant-negative SGK1 and PKB constructs Investigative ophthalmology & visual science Medium 15111600
2006 EAAC1 has a unique anti-apoptotic function independent of glutamate removal: during apoptotic stimuli, holocytochrome c synthetase (HCCS) translocates from mitochondria and suppresses XIAP (activating caspase-3). The N-terminus of EAAC1 binds HCCS, interfering with the HCCS-XIAP interaction and thereby maintaining XIAP activity and inhibiting caspase-3. This mechanism rescues PC12 cells from NGF deprivation and protects motor neurons from nerve injury. Co-immunoprecipitation of EAAC1 N-terminus with HCCS, binding competition assays (HCCS-XIAP interaction), caspase-3 activity assay, PC12 cell and motor neuron rescue experiments The EMBO journal High 16858406
2007 GTRAP3-18 negatively regulates neuronal glutathione synthesis by interacting with EAAC1 at the plasma membrane, reducing cysteine uptake. Increasing GTRAP3-18 at the plasma membrane (via methyl-β-cyclodextrin) decreases GSH and increases oxidative stress vulnerability; decreasing GTRAP3-18 with antisense oligonucleotides increases GSH. PKC-stimulated EAAC1 activity increase is blocked by elevated surface GTRAP3-18. HEK293 cell model, antisense oligonucleotide knockdown, methyl-β-cyclodextrin to increase surface GTRAP3-18, GSH measurement, oxidative stress assays, PKC activation Molecular pharmacology High 17646425
2011 GTRAP3-18 regulates neuronal glutathione levels in vivo by controlling EAAC1-mediated cysteine uptake. Increased GTRAP3-18 decreases GSH and increases oxidative stress vulnerability in vitro and in vivo; decreased GTRAP3-18 increases GSH levels in vitro and in vivo. In vitro cell culture and in vivo (rodent) experiments, GTRAP3-18 protein level manipulation, GSH measurement, oxidative stress vulnerability assays Amino acids Medium 21373771
2008 ARL6IP1 indirectly promotes EAAC1-mediated glutamate transport by binding directly to addicsin (GTRAP3-18/Arl6ip5), competing for addicsin binding to EAAC1. The hydrophobic region (aa 103-117) of addicsin is crucial for both Arl6ip1-addicsin heterodimer and addicsin homodimer formation. In the presence of PKC activation, ARL6IP1 overexpression increases EAAC1-mediated transport by increasing glutamate affinity (not Vmax). The addicsin Y110A/L112A mutant (lacking Arl6ip1 binding) abolishes this enhancement. Co-immunoprecipitation, alanine mutagenesis of addicsin binding region, glutamate transport assays, kinetic analysis, PKC activation with PMA The Journal of biological chemistry Medium 18684713
2012 EAAC1 is expressed in neuronal and glial mitochondria where it participates in glutamate-stimulated ATP production. EAAC1 physically interacts with the sodium/calcium exchanger NCX1 in mitochondria; NCX1 activity is essential for EAAC1-mediated glutamate-stimulated ATP synthesis. Antisense knockdown of either EAAC1 or NCX1 abolishes this mitochondrial metabolic response. Western blot, confocal microscopy, immunoelectron microscopy, luciferase-luciferin ATP assay, pharmacological blockers, EAAC1 and NCX1 antisense oligonucleotides, co-immunoprecipitation PloS one Medium 22479505
2019 SorCS2 acts as a sorting receptor that sustains EAAC1/EAAT3 cell surface expression to facilitate cysteine import and glutathione synthesis. Lack of SorCS2 depletes EAAT3 from the plasma membrane, impairs neuronal cysteine uptake, causes oxidative brain damage, and increases neuronal death and mortality during epilepsy in SorCS2-deficient mice. SorCS2-knockout mouse model, EAAT3 surface expression assay, cysteine uptake assay, glutathione measurement, oxidative stress and neuronal death quantification in epilepsy model Cell reports High 30840898
2017 EAAT3/SLC1A1 loss in the midbrain (but not striatum) reduces dopamine release in the dorsal striatum. Slc1a1-STOP mice show reduced extracellular dopamine, impaired locomotor and stereotypic responses to amphetamine, reduced D1 receptor binding in the dorsal striatum, and diminished OCD-like grooming behavior. Viral restoration of EAAT3 in the midbrain (but not striatum) partially rescues these phenotypes, consistent with a presynaptic dopaminergic role for EAAT3. STOP-cassette conditional knockout mouse, amphetamine locomotor and stereotypy assays, in vivo microdialysis for extracellular dopamine, D1 receptor autoradiography, immediate early gene induction assay, viral vector-mediated regional rescue PNAS High 28507136
2018 Mice with EAAT3 overexpression driven by CaMKIIα promoter (EAAT3glo/CMKII) display increased anxiety-like and repetitive behaviors, greater fear conditioning, and altered NMDA receptor subunit composition and NMDA-dependent synaptic plasticity at corticostriatal synapses. These behavioral effects are reversed by chronic fluoxetine or clomipramine treatment. Cre-dependent transgenic overexpression, behavioral assays (anxiety, repetitive behaviors, fear conditioning), electrophysiology at corticostriatal synapses, NMDA subunit biochemical analysis, pharmacological rescue Neuropsychopharmacology High 30622300
2001 PKC activation by phorbol ester inhibits EAAC1 in Xenopus oocytes by promoting its retrieval from the plasma membrane, reducing Imax with no change in Km. PMA simultaneously decreased membrane capacitance and increased cytosolic EAAC1 accumulation. This effect is PKC-mediated (blocked by PKC inhibitors; inactive 4α-PDD has no effect). Notably, this is opposite to the stimulatory PKC effect seen in C6 glioma cells, demonstrating cell-type specificity of PKC regulation. Xenopus oocyte expression system, [3H]L-glutamate uptake, dual electrode voltage clamp, PKC inhibitors, membrane capacitance measurement, EAAC1 protein localization Brain research Medium 11578612
2009 Wild-type PIP5K2A (phosphatidylinositol-4-phosphate 5-kinase IIα) increases EAAT3 transport activity and membrane abundance in Xenopus oocytes and HEK cells. The schizophrenia-associated mutant (N251S)PIP5K2A exerts a dominant inhibitory effect, decreasing EAAT3 membrane abundance and transport activity, even in the presence of wild-type PIP5K2A. Xenopus oocyte co-expression, dual electrode voltage clamp, confocal microscopy, chemiluminescence membrane protein quantification in HEK cells Psychopharmacology Medium 19644675
2010 AMP-activated protein kinase (AMPK) downregulates EAAT3 (and EAAT4) by reducing their membrane abundance. Constitutively active AMPK (γR70Q) or wild-type AMPK co-expressed with EAAT3 in Xenopus oocytes significantly decreases maximal glutamate-induced current (Ig) without changing Km; inactive AMPK (αK45R) has no effect. Xenopus oocyte expression, dual electrode voltage clamp, confocal microscopy for membrane abundance, Western blotting Journal of neurochemistry Medium 20218975
2012 mTOR coexpression significantly increases EAAT3 transport activity (glutamate-induced current) and EAAT3 membrane protein abundance in Xenopus oocytes; this effect is reversed by rapamycin (100 nM). The decay of transport current after brefeldin A treatment is similar with and without rapamycin, suggesting mTOR regulates delivery rather than retrieval of EAAT3. Xenopus oocyte co-expression, dual electrode voltage clamp, rapamycin pharmacology, brefeldin A carrier insertion block, chemiluminescence for membrane protein quantification Biochemical and biophysical research communications Medium 22483750
2013 Three alternative SLC1A1/EAAC1 mRNA isoforms (P2 internal promoter transcript, ex2skip lacking exon 2, ex11skip lacking exon 11) all inhibit glutamate uptake by the full-length EAAC1 transporter. Ex2skip and ex11skip isoforms partially colocalize with and physically interact with the full-length EAAC1 protein. Isoform cloning, co-immunoprecipitation, colocalization studies, glutamate uptake inhibition assays Translational psychiatry Medium 23695234
1997 EAAC1 protein is localized on the luminal (apical) membrane of S2 and S3 segments of proximal renal tubules, consistent with a role as the apical high-affinity glutamate transporter mediating reabsorption of acidic amino acids in the kidney beyond early S1 segments. In situ hybridization, immunofluorescence microscopy with anti-EAAC1 antibodies, Western blotting of kidney cortex and medulla fractions The American journal of physiology Medium 9435692
2000 EAAC1 is localized perisynaptically (outside the synaptic specialization) in dendritic membranes and cytoplasm of hippocampal neurons, with membrane-associated EAAC1 not intermingled with GluR2 within the synaptic complex. A significant presynaptic pool of EAAC1 also exists. EAAC1 is not at the postsynaptic density but is ideally positioned to regulate perisynaptic and presynaptic glutamate levels. Pre-embedding immunoelectron microscopy, post-embedding double-label immunogold localization, EAAC1 vs. GluR2 spatial mapping in rat hippocampus The Journal of comparative neurology Medium 10701825
2020 SLC1A1 actively recycles extracellular glutamate into lung cancer cells, which enhances the efficiency of cystine uptake via the cystine/glutamate antiporter Xc- and promotes glutathione biosynthesis. Depletion of SLC1A1 increases extracellular glutamate, inhibits cystine uptake, blocks GSH synthesis, and induces oxidative stress-mediated cell death. This is demonstrated by stable isotope-assisted metabolomics. SLC1A1 knockdown and overexpression, stable isotope-assisted metabolomics (cystine and glutamate flux measurement), extracellular glutamate measurement, GSH quantification, cell death assays Cancer research High 33229341
2022 SLC1A1, preferentially expressed in vascular endothelial cells, imports oncometabolite R-2-hydroxyglutarate (R-2-HG) from IDH1-mutant tumor microenvironment into endothelial cells and traffics it to mitochondria. R-2-HG via SLC1A1 promotes mitochondrial Na+/Ca2+ exchange, activates the mitochondrial respiratory chain, and fuels endothelial cell migration and tumor angiogenesis. SLC1A1 deficiency in mice abolishes mIDH1-promoted tumor angiogenesis. SLC1A1-knockout mice, tumor angiogenesis assays, R-2-HG uptake and subcellular fractionation, mitochondrial respiration assays, Ca2+ and Na+ flux measurements, endothelial migration assays Cell research High 35459936

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2006 Glutamate transporter gene SLC1A1 associated with obsessive-compulsive disorder. Archives of general psychiatry 236 16818866
2001 Modulation of the neuronal glutamate transporter EAAC1 by the interacting protein GTRAP3-18. Nature 187 11242046
2006 Association testing of the positional and functional candidate gene SLC1A1/EAAC1 in early-onset obsessive-compulsive disorder. Archives of general psychiatry 181 16818867
1998 EAAC1, a high-affinity glutamate tranporter, is localized to astrocytes and gabaergic neurons besides pyramidal cells in the rat cerebral cortex. Cerebral cortex (New York, N.Y. : 1991) 176 9542890
2012 The density of EAAC1 (EAAT3) glutamate transporters expressed by neurons in the mammalian CNS. The Journal of neuroscience : the official journal of the Society for Neuroscience 169 22539860
2007 Association of the SLC1A1 glutamate transporter gene and obsessive-compulsive disorder. American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics 135 17894418
2010 Aberrant Rab11-dependent trafficking of the neuronal glutamate transporter EAAC1 causes oxidative stress and cell death in Huntington's disease. The Journal of neuroscience : the official journal of the Society for Neuroscience 130 20357106
2005 Individual subunits of the glutamate transporter EAAC1 homotrimer function independently of each other. Biochemistry 127 16128593
2015 Glutathione in Cellular Redox Homeostasis: Association with the Excitatory Amino Acid Carrier 1 (EAAC1). Molecules (Basel, Switzerland) 121 26007177
2000 Differential synaptic localization of the glutamate transporter EAAC1 and glutamate receptor subunit GluR2 in the rat hippocampus. The Journal of comparative neurology 121 10701825
2010 N-acetylcysteine prevents loss of dopaminergic neurons in the EAAC1-/- mouse. Annals of neurology 119 21446024
2006 The neuronal excitatory amino acid transporter EAAC1/EAAT3: does it represent a major actor at the brain excitatory synapse? Journal of neurochemistry 118 16800850
2004 Rapid trafficking of the neuronal glutamate transporter, EAAC1: evidence for distinct trafficking pathways differentially regulated by protein kinase C and platelet-derived growth factor. The Journal of biological chemistry 117 15197183
2002 Increased expression of the neuronal glutamate transporter (EAAT3/EAAC1) in hippocampal and neocortical epilepsy. Epilepsia 112 11906504
1996 Rapid stimulation of EAAC1-mediated Na+-dependent L-glutamate transport activity in C6 glioma cells by phorbol ester. Journal of neurochemistry 111 8764574
1996 Comparison of Na+-dependent glutamate transport activity in synaptosomes, C6 glioma, and Xenopus oocytes expressing excitatory amino acid carrier 1 (EAAC1). Molecular pharmacology 109 8643086
2010 Loss-of-function mutations in the glutamate transporter SLC1A1 cause human dicarboxylic aminoaciduria. The Journal of clinical investigation 102 21123949
2000 Platelet-derived growth factor rapidly increases activity and cell surface expression of the EAAC1 subtype of glutamate transporter through activation of phosphatidylinositol 3-kinase. The Journal of biological chemistry 101 10671571
2001 Transient focal cerebral ischemia down-regulates glutamate transporters GLT-1 and EAAC1 expression in rat brain. Neurochemical research 88 11513475
1999 Glutamate transporter EAAC1 is expressed in neurons and glial cells in the rat nervous system. Glia 88 10417812
1997 Immunohistochemical localization of the neuron-specific glutamate transporter EAAC1 (EAAT3) in rat brain and spinal cord revealed by a novel monoclonal antibody. Brain research 87 9409715
2002 Regulation of the neuronal glutamate transporter excitatory amino acid carrier-1 (EAAC1) by different protein kinase C subtypes. Molecular pharmacology 82 12237337
2020 Dysregulated Glutamate Transporter SLC1A1 Propels Cystine Uptake via Xc- for Glutathione Synthesis in Lung Cancer. Cancer research 80 33229341
2013 Meta-analysis of association between obsessive-compulsive disorder and the 3' region of neuronal glutamate transporter gene SLC1A1. American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics 76 23606572
1997 Non-synaptic localization of the glutamate transporter EAAC1 in cultured hippocampal neurons. The European journal of neuroscience 76 9383213
1996 Characterization and distribution of the neuronal glutamate transporter EAAC1 in rat brain. The American journal of physiology 74 8772431
2013 CNV analysis in a large schizophrenia sample implicates deletions at 16p12.1 and SLC1A1 and duplications at 1p36.33 and CGNL1. Human molecular genetics 73 24163246
2009 Association of the glutamate transporter gene SLC1A1 with atypical antipsychotics-induced obsessive-compulsive symptoms. Archives of general psychiatry 73 19884611
2013 Changes in the expression of the glutamate transporter EAAT3/EAAC1 in health and disease. Cellular and molecular life sciences : CMLS 70 24162932
2001 Na+ dependent glutamate transporters (EAAT1, EAAT2, and EAAT3) in primary astrocyte cultures: effect of oxidative stress. Brain research 69 11730698
2013 Soluble oligomers of amyloid-β cause changes in redox state, DNA methylation, and gene transcription by inhibiting EAAT3 mediated cysteine uptake. Journal of Alzheimer's disease : JAD 68 23579332
2011 Comprehensive family-based association study of the glutamate transporter gene SLC1A1 in obsessive-compulsive disorder. American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics 66 21445956
2004 Pharmacological characterization of human excitatory amino acid transporters EAAT1, EAAT2 and EAAT3 in a fluorescence-based membrane potential assay. Biochemical pharmacology 60 15135308
2007 Reticulon RTN2B regulates trafficking and function of neuronal glutamate transporter EAAC1. The Journal of biological chemistry 58 18096700
2018 P2X4-receptor participates in EAAT3 regulation via BDNF-TrkB signaling in a model of trigeminal allodynia. Molecular pain 57 30146940
2003 Phorbol myristate acetate-dependent interaction of protein kinase Calpha and the neuronal glutamate transporter EAAC1. The Journal of neuroscience : the official journal of the Society for Neuroscience 55 12843260
2001 Genomic organization of the SLC1A1/EAAC1 gene and mutation screening in early-onset obsessive-compulsive disorder. Molecular psychiatry 55 11317217
2017 OCD candidate gene SLC1A1/EAAT3 impacts basal ganglia-mediated activity and stereotypic behavior. Proceedings of the National Academy of Sciences of the United States of America 54 28507136
2013 Influence of polymorphisms in genes SLC1A1, GRIN2B, and GRIK2 on clozapine-induced obsessive-compulsive symptoms. Psychopharmacology 54 23660601
2022 SLC1A1-mediated cellular and mitochondrial influx of R-2-hydroxyglutarate in vascular endothelial cells promotes tumor angiogenesis in IDH1-mutant solid tumors. Cell research 51 35459936
2008 Expression and distribution of 'high affinity' glutamate transporters GLT1, GLAST, EAAC1 and of GCPII in the rat peripheral nervous system. Journal of anatomy 51 19014361
2013 Involvement of pGluR1, EAAT2 and EAAT3 in offspring depression induced by prenatal stress. Neuroscience 50 23694703
2004 Retinal colocalization and in vitro interaction of the glutamate transporter EAAT3 and the serum- and glucocorticoid-inducible kinase SGK1 [correction]. Investigative ophthalmology & visual science 48 15111600
2000 Altered expression of the glutamate transporter EAAC1 in neurons and immature oligodendrocytes after transient forebrain ischemia. Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 46 10779012
2021 SLC1A1 mediated glutamine addiction and contributed to natural killer T-cell lymphoma progression with immunotherapeutic potential. EBioMedicine 45 34628354
1997 Localization of the high-affinity glutamate transporter EAAC1 in rat kidney. The American journal of physiology 45 9435692
2010 EAAC1 gene deletion alters zinc homeostasis and exacerbates neuronal injury after transient cerebral ischemia. The Journal of neuroscience : the official journal of the Society for Neuroscience 44 21084597
2001 Inhibition of the glutamate transporter EAAC1 expressed in Xenopus oocytes by phorbol esters. Brain research 44 11578612
2007 Prenatal exposure to the cannabinoid receptor agonist WIN 55,212-2 increases glutamate uptake through overexpression of GLT1 and EAAC1 glutamate transporter subtypes in rat frontal cerebral cortex. Neuropharmacology 43 17631920
2011 Modulation of neuronal glutathione synthesis by EAAC1 and its interacting protein GTRAP3-18. Amino acids 42 21373771
2007 Association study of polymorphisms in the glutamate transporter genes SLC1A1, SLC1A3, and SLC1A6 with schizophrenia. American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics 42 17221839
2000 Modulation of glutamate transporters (GLAST, GLT-1 and EAAC1) in the rat cerebellum following portocaval anastomosis. Brain research 42 10719077
2011 Interaction between genetic variants of DLGAP3 and SLC1A1 affecting the risk of atypical antipsychotics-induced obsessive-compulsive symptoms. American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics 41 21990008
2008 Detergent-insoluble EAAC1/EAAT3 aberrantly accumulates in hippocampal neurons of Alzheimer's disease patients. Brain pathology (Zurich, Switzerland) 41 18624794
2006 EAAC1 is expressed in rat and human prostate epithelial cells; functions as a high-affinity L-aspartate transporter; and is regulated by prolactin and testosterone. BMC biochemistry 41 16566829
2006 Unique anti-apoptotic activity of EAAC1 in injured motor neurons. The EMBO journal 41 16858406
2002 The effects of lidocaine on the activity of glutamate transporter EAAT3: the role of protein kinase C and phosphatidylinositol 3-kinase. Anesthesia and analgesia 41 12401608
2005 Downregulation of spinal glutamate transporter EAAC1 following nerve injury is regulated by central glucocorticoid receptors in rats. Pain 40 16360273
2005 A carboxyl-terminal determinant of the neuronal glutamate transporter, EAAC1, is required for platelet-derived growth factor-dependent trafficking. The Journal of biological chemistry 40 16368696
2018 Mn Inhibits GSH Synthesis via Downregulation of Neuronal EAAC1 and Astrocytic xCT to Cause Oxidative Damage in the Striatum of Mice. Oxidative medicine and cellular longevity 38 30228854
2010 A screen of SLC1A1 for OCD-related alleles. American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics 38 19569082
2005 Specificity of antibodies: unexpected cross-reactivity of antibodies directed against the excitatory amino acid transporter 3 (EAAT3). Neuroscience 38 16344142
2018 Behavioral and synaptic alterations relevant to obsessive-compulsive disorder in mice with increased EAAT3 expression. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 37 30622300
2013 Deletion at the SLC1A1 glutamate transporter gene co-segregates with schizophrenia and bipolar schizoaffective disorder in a 5-generation family. American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics 37 23341099
2007 Influence of environmental enrichment on steady-state mRNA levels for EAAC1, AMPA1 and NMDA2A receptor subunits in rat hippocampus. Brain research 36 17854777
2019 SorCS2 Controls Functional Expression of Amino Acid Transporter EAAT3 and Protects Neurons from Oxidative Stress and Epilepsy-Induced Pathology. Cell reports 34 30840898
2012 Physical and functional interaction of NCX1 and EAAC1 transporters leading to glutamate-enhanced ATP production in brain mitochondria. PloS one 34 22479505
2007 C6 glioma cells differentiated by retinoic acid overexpress the glutamate transporter excitatory amino acid carrier 1 (EAAC1). Neuroscience 34 18207650
2006 Syntaxin 1A promotes the endocytic sorting of EAAC1 leading to inhibition of glutamate transport. Journal of cell science 34 16959903
2002 The regionalization of PepT1, NBAT and EAAC1 transporters in the small intestine of rats are unchanged from birth to adulthood. The Journal of nutrition 34 11983829
2017 Human miR-26a-5p regulates the glutamate transporter SLC1A1 (EAAT3) expression. Relevance in multiple sclerosis. Biochimica et biophysica acta. Molecular basis of disease 33 28962897
2007 Regulation of glutathione synthesis via interaction between glutamate transport-associated protein 3-18 (GTRAP3-18) and excitatory amino acid carrier-1 (EAAC1) at plasma membrane. Molecular pharmacology 33 17646425
2006 TNFR1 mediates increased neuronal membrane EAAT3 expression after in vivo cerebral ischemic preconditioning. Neuroscience 31 16442237
2005 Evidence that Akt mediates platelet-derived growth factor-dependent increases in activity and surface expression of the neuronal glutamate transporter, EAAC1. Neuropharmacology 31 16182322
2005 Differential modulation of the glutamate transporters GLT1, GLAST and EAAC1 by docosahexaenoic acid. Brain research 30 15777760
2004 Glial soluble factors regulate the activity and expression of the neuronal glutamate transporter EAAC1: implication of cholesterol. Journal of neurochemistry 30 15009653
2002 Cytoskeleton-related trafficking of the EAAC1 glutamate transporter after activation of the G(q/11)-coupled neurotensin receptor NTS1. FEBS letters 30 12123836
2010 Down-regulation of Na+-coupled glutamate transporter EAAT3 and EAAT4 by AMP-activated protein kinase. Journal of neurochemistry 29 20218975
2008 Modulation of the neural glutamate transporter EAAC1 by the addicsin-interacting protein ARL6IP1. The Journal of biological chemistry 29 18684713
2012 Neurosteroid allopregnanolone regulates EAAC1-mediated glutamate uptake and triggers actin changes in Schwann cells. Journal of cellular physiology 28 21688266
2012 Transient striatal GLT-1 blockade increases EAAC1 expression, glutamate reuptake, and decreases tyrosine hydroxylase phosphorylation at ser(19). Experimental neurology 28 22285253
2009 PIP5K2A-dependent regulation of excitatory amino acid transporter EAAT3. Psychopharmacology 28 19644675
2003 Methyl-beta-cyclodextrin but not retinoic acid reduces EAAT3-mediated glutamate uptake and increases GTRAP3-18 expression. Journal of neurochemistry 28 12562531
2020 Estrogen and progesterone attenuate glutamate neurotoxicity via regulation of EAAT3 and GLT-1 in a rat model of ischemic stroke. Iranian journal of basic medical sciences 27 33149869
2016 EAAT3 promotes amino acid transport and proliferation of porcine intestinal epithelial cells. Oncotarget 27 27231847
2015 Roles of the NMDA Receptor and EAAC1 Transporter in the Modulation of Extracellular Glutamate by Low and High Affinity AMPA Receptors in the Cerebellum in Vivo: Differential Alteration in Chronic Hyperammonemia. ACS chemical neuroscience 27 26428532
2013 Isoforms of the neuronal glutamate transporter gene, SLC1A1/EAAC1, negatively modulate glutamate uptake: relevance to obsessive-compulsive disorder. Translational psychiatry 26 23695234
2010 Glutamate transporter gene (SLC1A1) single nucleotide polymorphism (rs301430) and repetitive behaviors and anxiety in children with autism spectrum disorder. Journal of autism and developmental disorders 26 20155310
2006 A dominant-negative variant of SNAP-23 decreases the cell surface expression of the neuronal glutamate transporter EAAC1 by slowing constitutive delivery. Neurochemistry international 26 16516346
2005 Effects of chronic exposure to ethanol on glutamate transporter EAAT3 expressed in Xenopus oocytes: evidence for protein kinase C involvement. Alcoholism, clinical and experimental research 26 16340463
2003 Content of ileal EAAC1 and hepatic GLT-1 high-affinity glutamate transporters is increased in growing vs. nongrowing lambs, paralleling increased tissue D- and L-glutamate, plasma glutamine, and alanine concentrations. Journal of animal science 26 12723093
2012 Regulation of the glutamate transporter EAAT3 by mammalian target of rapamycin mTOR. Biochemical and biophysical research communications 25 22483750
1998 Regional and cellular expression of glial (GLT1) and neuronal (EAAC1) glutamate transporter proteins in ovine fetal brain. Neuroscience 25 9681956
2011 Association of SNPs linked to increased expression of SLC1A1 with schizophrenia. American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics 24 22095641
2017 Strong association of SLC1A1 and DPF3 gene variants with idiopathic male infertility in Han Chinese. Asian journal of andrology 23 27232852
2016 Decreased cysteine uptake by EAAC1 gene deletion exacerbates neuronal oxidative stress and neuronal death after traumatic brain injury. Amino acids 23 27040821
2015 Exercise-Mediated Increase in Nigral Tyrosine Hydroxylase Is Accompanied by Increased Nigral GFR-α1 and EAAC1 Expression in Aging Rats. ACS chemical neuroscience 23 26599339
2008 Evidence for potential relationship between SLC1A1 and a putative genetic linkage region on chromosome 14q to obsessive-compulsive disorder with compulsive hoarding. American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics 23 18286588
2004 Prenatal cannabinoid exposure down- regulates glutamate transporter expressions (GLAST and EAAC1) in the rat cerebellum. Developmental neuroscience 23 15509898
2002 Lack of glutamate transporter EAAC1 in the epididymis of infertile c-ros receptor tyrosine-kinase deficient mice. Journal of andrology 23 12399522

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