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FLASH GENE

Symbol

SLC1A1

contributors: mct/npt/shn - updated : 17-04-2016

HGNC name	solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1
HGNC id	10939

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

EXPRESSION

Type

widely

expressed in

(based on citations)

organ(s)

System Organ level 1 Organ level 2 Organ level 3 Organ level 4 Level Pubmed Species Stage Rna symbol Nervous brain forebrain cerebral cortex   highly Homo sapiens   brain forebrain cerebral cortex frontal cortex specific Homo sapiens   brain limbic system hippocampus   lowly Homo sapiens   brain hindbrain cerebellum   lowly Homo sapiens   brain       highly Homo sapiens   ganglia       moderately Homo sapiens Reproductive female system placenta     moderately Homo sapiens Respiratory lung       moderately Homo sapiens Urinary kidney tubule convoluted tubule proximal tubule   Homo sapiens

cell lineage

cell lines

fluid/secretion

at STAGE

PROTEIN

PHYSICAL PROPERTIES

STRUCTURE

motifs/domains	10 transmembrane spanning segments (10TM)
	six N terminal and cytoplasmic N and C termini

HOMOLOGY

interspecies	ortholog to Slc1a1, Mus musculus
	ortholog to Slc1a1, Rattus norvegicus
	ortholog to SLC1A1, Pan troglodytes

Homologene

FAMILY

sodium : dicarboxylate (SDF) symporter (tc 2.a.23) family

CATEGORY

transport carrier

SUBCELLULAR LOCALIZATION	plasma membrane
	intracellular
	intracellular,cytoplasm,organelle,mitochondria
text	expressed in neuronal and glial mitochondria where it participates in glutamate-stimulated ATP production

basic FUNCTION	glial high affinity glutamate transporter, Na and K dependent
	play an essential role in regulating temporal and spatial glutamate concentration in the synaptic cleft
	playing an essential role for terminating the postsynaptic action of glutamate by rapidly removing released glutamate from the synaptic cleft
	acting as a symport by cotransporting sodium
	important for zinc homeostasis and neuronal antioxidant function under ischemic conditions
	neuronal transporters (SLC1A1, SLC1A6, and SLC1A7) appear to have additional functions in regulating and processing cellular excitability

CELLULAR PROCESS

PHYSIOLOGICAL PROCESS

text	a neuronal glutamate and cysteine transporter

PATHWAY

metabolism

signaling

a component

INTERACTION

DNA

RNA

small molecule

protein	GTRAP3-18
	PKCalpha
	physical interaction between SLC1A1 and SLC8A1 both in neuronal and glial mitochondria, and SLC8A1 is an essential modulator of this glutamate transporter
	KL is a novel, powerful regulator of the excitatory amino acid transporters SLC1A1, SLC1A6
	ARL6IP5 is a negative modulator of the neural glutamate transporter excitatory amino acid carrier 1 (SLC1A1) (
	both, STK39 and OXSR1 are negative regulators of SLC1A1 activity
	CAV1 is a powerful negative regulator of the excitatory glutamate transporters SLC1A1, SLC1A2, SLC1A3, SLC1A6
	SORCS2 acts as sorting receptor that sustains cell surface expression of the neuronal amino acid transporter SLC1A1 to facilitate import of cysteine, required for synthesis of the reactive oxygen species scavenger glutathione

cell & other

REGULATION

activated by

protein kinase C, PKC

Other	its trafficking on and off the plasma membrane is regulated by CAV1
	regulation by expression and activation of delta-opioid receptor

ASSOCIATED DISORDERS

corresponding disease(s)

related resource

MITOP database

Susceptibility

to Obsessive-Compulsive Disorder

Variant & Polymorphism other	polymorphism increasing the risk of obsessive-compulsive disorder

Candidate gene
Marker
Therapy target	Treatment of the EAAC1(-/-) mice with N-acetyl cysteine restored neuronal glutathione concentrations, normalized basal zinc levels, reduced ischemia-induced zinc translocation, superoxide production, and neuron death

ANIMAL & CELL MODELS

EAAC1(-/-) mice subjected to transient cerebral ischemia exhibited twice as much hippocampal neuronal death, elevated vesicular and cytosolic zinc concentrations in hippocampal CA1 neurons and an increased zinc translocation to postsynaptic neurons after ischemia