SLC17A9 CRISPR/Cas9 KO Plasmid (m): sc-432833
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SLC17A9 CRISPR/Cas9 Knockout (KO) Plasmid (m) 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 SLC17A9 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 | |
SLC17A9 CRISPR/Cas9 KO Plasmid (m) | sc-432833 | 20 µg | $397.00 |
Overview
Slc17a9 encodes SLC17A9, a vesicular nucleotide transporter (VNUT) that loads ATP and other nucleotides into secretory vesicles, enabling regulated purinergic signaling. By controlling vesicular ATP content, SLC17A9 influences exocytosis-dependent communication that engages P2X/P2Y receptor pathways and downstream Ca²⁺- and MAPK-linked responses in neural and immune contexts. This transport activity supports processes including neurotransmission, microglial activation, and inflammatory mediator release, making Slc17a9 a useful node for studying neuroimmune crosstalk and sterile inflammation. Dysregulated vesicular ATP handling and purinergic tone have been implicated in pain signaling, neuroinflammation, and tissue injury responses, positioning Slc17a9 as a mechanistically relevant target for pathway interrogation in mouse models.
SLC17A9 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Slc17a9 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Slc17a9 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 Slc17a9 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 SLC17A9 protein expression.
This CRISPR knockout system enables efficient generation of Slc17a9-deficient cell models for investigation of SLC17A9 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Slc17a9 exon(s) critical for SLC17A9 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 Slc17a9 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SLC17A9 CRISPR/Cas9 KO Plasmid (m) and SLC17A9 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Slc17a9 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SLC17A9 HDR Plasmid (m) and SLC17A9 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Slc17a9 homology arms to support homology-directed repair at defined Slc17a9 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.