Cystinosin CRISPR/Cas9 KO Plasmid (m): sc-429900
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Cystinosin 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 Cystinosin 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 | |
Cystinosin CRISPR/Cas9 KO Plasmid (m) | sc-429900 | 20 µg | $397.00 |
Overview
Ctns encodes cystinosin, a lysosomal H+-driven cystine transporter that mediates cystine efflux from the lysosomal lumen to the cytosol, linking lysosomal transport to cellular redox balance and amino acid homeostasis. Loss of cystinosin activity perturbs lysosomal function, promotes cystine accumulation, and alters pathways involved in autophagy–lysosome dynamics, oxidative stress responses, and metabolic adaptation. In mouse systems, Ctns disruption is widely used to model mechanisms underlying cystine storage phenotypes and to examine how lysosomal transport defects reshape cellular stress signaling. These processes are relevant to understanding how lysosome-centered trafficking and degradation networks influence tissue homeostasis in renal, ocular, and immune-relevant cell types.
Cystinosin CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Ctns gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ctns 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 Ctns 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 Cystinosin protein expression.
This CRISPR knockout system enables efficient generation of Ctns-deficient cell models for investigation of Cystinosin signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Ctns exon(s) critical for Cystinosin 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 Ctns genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Cystinosin CRISPR/Cas9 KO Plasmid (m) and Cystinosin CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ctns locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Cystinosin HDR Plasmid (m) and Cystinosin HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ctns homology arms to support homology-directed repair at defined Ctns 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.