GLAST peptide


Antigenic peptide from the glutamate transporter, GLAST

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Catalogue number crb1200276
Protein ID UniProtKB - P43003
Aliases SLC1A3, Solute carrier family 1 (glial high-affinity glutamate transporter), member 3, GLAST GLutamate ASpartate Transporter, EAAT1 Excitatory Amino Acid Transporter 1
Cross-Reactivity Rat, Mouse
Disease Area Neurodegenerative diseases
Family Sodium:dicarboxylate (SDF) symporter family
Storage -20°c

Martin, C., Houitte, D., Guillermier, M., Petit, F., Bonvento, G. and Gurden, H. (2012). Alteration of sensory-evoked metabolic and oscillatory activities in the olfactory bulb of GLAST-deficient mice. Front Neural Circuits, 6. PMID: 22291618


Perkins, E., Clarkson, Y., Suminaite, D., Lyndon, A., Tanaka, K., Rothstein, J., Skehel, P., Wyllie, D. and Jackson, M. (2018). Loss of cerebellar glutamate transporters EAAT4 and GLAST differentially affects the spontaneous firing pattern and survival of Purkinje cells. Hum Mol Genet, 27(15), 2614-2627. PMID: 29741614


Siddiqi, F., Chen, F., Aron, A., Fiondella, C., Patel, K. and LoTurco, J. (2012). Fate Mapping by PiggyBac Transposase Reveals That Neocortical GLAST+ Progenitors Generate More Astrocytes Than Nestin+ Progenitors in Rat Neocortex. Cereb Cortex, 24(2), 508-520. PMID: 23118195

Specificity Protein
GLAST/ EAAT-1 (GLutamate–ASpartate Transporter/ Excitatory amino acid transporter 1) (rodent/human nomenclature) is a sodium-dependent plasma membrane glutamate transporter expressed exclusively by astrocytes in the cerebellum and present at high densities near excitatory synapses. The cerebellum is the region of the brain essential for maintaining postural control and coordination of voluntary muscle movement.
Glutamate transporters regulate glutamate receptors and limit glutamate accumulation to prevent neurotoxicity whilst ensuring accurate synaptic communication. GLAST is the major transporter expressed during development.

Loss of GLAST/EAAT-1 has been linked to the pathogenesis of several disorders affecting the motor system including several subtypes of spinocerebellar ataxia (SCA); SCA1, SCA5, SCA7, episodic ataxia type 6, spinal muscular atrophy and fragile X associated tremor/ataxia syndrome. Furthermore, disrupted GLAST/EAAT-1 has been associated with schizophrenia and cerebellar dysfunction and also is linked to the pathophysiology of Alzheimer’s disease, autism and other cognitive and neuropsychiatric disorders

GLAST peptide

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