EAAT1 Antibody [B6P21] | Primary Antibodies

Application: Reactivity: Mouse, Rat, Human

Lane 1: Mouse brain, Lane 2: Rat brain

Usage Information

Dilution
WB1:1000 - 1:10000 IHC1:50 - 1:1000 IF1:50

Application
WB, IHC, IF

Reactivity
Mouse, Rat, Human

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
143 kDa,26 kDa,59 kDa 143 kDa,26 kDa,59 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight.

Positive Control	Human cerebellum; Mouse brain; Mouse hippocampus; Rat hippocampus; Rat brain
Negative Control	Mouse brain (boiled)

Datasheet & SDS

Biological Description

Specificity
EAAT1 Antibody [B6P21] detects endogenous levels of total EAAT1 protein.

Clone
B6P21

Synonym(s)
EAAT1; GLAST; GLAST1; SLC1A3; Excitatory amino acid transporter 1; Sodium-dependent glutamate/aspartate transporter 1; Solute carrier family 1 member 3; GLAST-1

Background
EAAT1 (excitatory amino acid transporter 1, also known as GLAST1 or SLC1A3) is a glial-predominant Na⁺/K⁺-coupled glutamate and aspartate symporter that contributes a modest portion of forebrain glutamate uptake compared to the dominant EAAT2/GLT-1 isoform. It functions as a homotrimeric elevator, with each protomer composed of a rigid trimerization scaffold domain formed by multiple transmembrane helices and a mobile transport domain that elevates substrates across the membrane. The structure also includes a glycosylated extracellular loop and an intracellular C-terminal tail containing PKC phosphorylation sites, which regulate transporter trafficking and activity. The transporter’s operating stoichiometry generates a net positive charge influx per transport cycle and involves a sequence of substrate and ion binding events: Na⁺ binds first at well-defined sites, priming the transporter for glutamate binding through a network of coordinated residues and hydrogen bonds. This triggers an elevator-like descent of the transport domain, opening a gate and enabling K⁺ countertransport to reset the transporter for another cycle. Astrocytes can rapidly upregulate surface expression of EAAT1 in response to glutamate via PKC and NF-κB-dependent trafficking, providing synaptic glutamate buffering that prevents NMDA and AMPA receptor overactivation and supports glial metabolic processes. Reactive astrocytes and microglia increase EAAT1 expression after ischemia to protect neurons, while chronic EAAT1 loss elevates extrasynaptic glutamate, contributing to neurodegeneration in ALS, epilepsy, and mood disorders.

Background

EAAT1 (excitatory amino acid transporter 1, also known as GLAST1 or SLC1A3) is a glial-predominant Na⁺/K⁺-coupled glutamate and aspartate symporter that contributes a modest portion of forebrain glutamate uptake compared to the dominant EAAT2/GLT-1 isoform. It functions as a homotrimeric elevator, with each protomer composed of a rigid trimerization scaffold domain formed by multiple transmembrane helices and a mobile transport domain that elevates substrates across the membrane. The structure also includes a glycosylated extracellular loop and an intracellular C-terminal tail containing PKC phosphorylation sites, which regulate transporter trafficking and activity. The transporter’s operating stoichiometry generates a net positive charge influx per transport cycle and involves a sequence of substrate and ion binding events: Na⁺ binds first at well-defined sites, priming the transporter for glutamate binding through a network of coordinated residues and hydrogen bonds. This triggers an elevator-like descent of the transport domain, opening a gate and enabling K⁺ countertransport to reset the transporter for another cycle. Astrocytes can rapidly upregulate surface expression of EAAT1 in response to glutamate via PKC and NF-κB-dependent trafficking, providing synaptic glutamate buffering that prevents NMDA and AMPA receptor overactivation and supports glial metabolic processes. Reactive astrocytes and microglia increase EAAT1 expression after ischemia to protect neurons, while chronic EAAT1 loss elevates extrasynaptic glutamate, contributing to neurodegeneration in ALS, epilepsy, and mood disorders.

References
https://pubmed.ncbi.nlm.nih.gov/25972039/ https://pubmed.ncbi.nlm.nih.gov/20708631/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%