GABA T-1 CRISPR/Cas9 KO Plasmid (h): sc-411007
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GABA T-1 CRISPR/Cas9 Knockout (KO) Plasmid (h) is a pool of plasmids, each encoding Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed for maximum knockout efficiency using sequences derived from the GeCKO v2 library
- gRNA sequences direct Cas9 to induce site-specific double-strand breaks (DSBs) in the GABA T-1 genomic locus, resulting in gene knockout through non-homologous end joining (NHEJ)
- The puromycin resistance and RFP genes are flanked by LoxP sites, enabling removal of selection markers via Cre recombinase (Cre Vector: sc-418923) after establishing stable knockout cell lines
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GABA T-1 CRISPR/Cas9 KO Plasmid (h) | sc-411007 | 20 µg | $397.00 |
Overview
SLC6A1 encodes the human GABA transporter 1 (GABA T-1), a high-affinity Na+/Cl−-dependent plasma membrane transporter that clears γ-aminobutyric acid (GABA) from synaptic and extrasynaptic spaces to shape inhibitory neurotransmission. By regulating GABA reuptake, GABA T-1 influences neuronal excitability, synaptic timing, and network oscillations, linking transporter activity to neurotransmitter cycling and ion-coupled transport processes. SLC6A1 dysfunction is associated with neurodevelopmental and epilepsy-related phenotypes, and altered GABA homeostasis has been implicated in broader mechanisms of cortical circuit imbalance. Experimental perturbation of SLC6A1 supports pathway-level studies of inhibitory signaling, receptor activation dynamics, and compensation by related solute carrier transporters.
GABA T-1 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the SLC6A1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the SLC6A1 together with the Streptococcus pyogenes Cas9 nuclease. The plasmids also encode GFP, allowing fluorescent identification and enrichment of successfully transfected cells by fluorescence microscopy or flow cytometry.
The multi-guide design increases the likelihood of generating insertions or deletions (indels) that disrupt the SLC6A1 open reading frame following Cas9-mediated double-strand break formation. DNA breaks introduced by the CRISPR/Cas9 system are repaired through endogenous non-homologous end joining (NHEJ) pathways, frequently resulting in frameshift mutations that abolish GABA T-1 protein expression.
This CRISPR knockout system enables efficient generation of SLC6A1-deficient cell models for investigation of GABA T-1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting SLC6A1 exon(s) critical for GABA T-1 function
- Co-expression of SpCas9 and sgRNA from a single plasmid for simplified delivery
- GFP reporter for identification of transfected cells
- Pool of plasmids targeting multiple SLC6A1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by GABA T-1 CRISPR/Cas9 KO Plasmid (h) and GABA T-1 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the SLC6A1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by GABA T-1 HDR Plasmid (h) and GABA T-1 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by SLC6A1 homology arms to support homology-directed repair at defined SLC6A1 target sites corresponding to the CRISPR/Cas9 KO designs. HDR donor availability may vary. See Related Products for availability.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.