SLC1A2 (solute carrier family 1 member 2) is a membrane-bound transporter critical for clearing extracellular glutamate in the central nervous system. By cotransporting sodium and glutamate, it terminates synaptic signaling and prevents excitotoxicity . Mutations or reduced expression of SLC1A2 are implicated in neurological disorders such as amyotrophic lateral sclerosis (ALS) and epilepsy .
The SLC1A2-FITC antibody is optimized for:
Immunofluorescence (IF): Direct visualization of SLC1A2 in brain tissue sections or cultured cells.
Western Blot (WB): Detection of SLC1A2 in lysates (dilution: 1:500–1:5000) .
Immunohistochemistry (IHC): Localization in paraffin-embedded tissue (dilution: 1:20–1:200) .
Specificity: Targets the extracellular domain of SLC1A2, minimizing cross-reactivity with intracellular epitopes .
Sensitivity: Detects SLC1A2 in human brain tissue homogenates and cell lines .
Compatibility: Works with standard protocols for FITC-based fluorescence microscopy .
Amyotrophic Lateral Sclerosis (ALS): Reduced SLC1A2 expression correlates with disease progression. FITC-conjugated antibodies enable colocalization studies with markers of neurodegeneration (e.g., TDP-43) .
Epilepsy and Neuroinflammation: SLC1A2 downregulation in astrocytes exacerbates glutamate toxicity. IF studies using this antibody track transporter dynamics in seizure models .
Regulation: SLC1A2 activity is modulated by post-translational modifications (e.g., phosphorylation). Fluorescence-based assays with FITC-conjugated antibodies monitor transporter trafficking in live cells .