Y+LAT1 CRISPR/Cas9 KO Plasmid (h): sc-404403
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Y+LAT1 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 Y+LAT1 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 | |
Y+LAT1 CRISPR/Cas9 KO Plasmid (h) | sc-404403 | 20 µg | $397.00 |
Overview
SLC7A7 encodes Y+LAT1, a light-chain subunit of the heteromeric amino acid transporter system y+L that partners with SLC3A2 (4F2hc/CD98) to mediate exchange of cationic amino acids such as lysine and arginine with neutral amino acids across the plasma membrane. This transporter activity supports cellular nitrogen balance and links amino acid availability to metabolic homeostasis and nutrient-sensing processes. Y+LAT1 function is especially relevant in epithelial and immune contexts where amino acid flux influences growth and signaling outputs. Pathogenic disruption of SLC7A7 is associated with lysinuric protein intolerance, connecting Y+LAT1-dependent transport defects to systemic amino acid imbalance and downstream inflammatory complications.
Y+LAT1 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the SLC7A7 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the SLC7A7 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 SLC7A7 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 Y+LAT1 protein expression.
This CRISPR knockout system enables efficient generation of SLC7A7-deficient cell models for investigation of Y+LAT1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting SLC7A7 exon(s) critical for Y+LAT1 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 SLC7A7 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Y+LAT1 CRISPR/Cas9 KO Plasmid (h) and Y+LAT1 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the SLC7A7 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Y+LAT1 HDR Plasmid (h) and Y+LAT1 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by SLC7A7 homology arms to support homology-directed repair at defined SLC7A7 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.