cathepsin S CRISPR/Cas9 KO Plasmid (m): sc-419881
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- cathepsin S 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 cathepsin S 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
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: cathepsin S Antibody (E-3): sc-271619
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
cathepsin S CRISPR/Cas9 KO Plasmid (m) | sc-419881 | 20 µg | $397.00 |
Overview
Ctss encodes mouse cathepsin S, a lysosomal cysteine protease with prominent expression in antigen-presenting cells where it drives proteolytic processing of internalized proteins. Cathepsin S is a key component of the MHC class II antigen presentation pathway by cleaving the invariant chain and enabling peptide loading, linking endolysosomal proteostasis to adaptive immune activation. Beyond antigen processing, cathepsin S contributes to extracellular matrix turnover and inflammatory signaling in myeloid lineages, supporting studies of leukocyte trafficking and tissue remodeling. Dysregulated CTSS activity has been associated with immune-mediated pathology and chronic inflammatory states, motivating mechanistic research in immunology and inflammation models.
cathepsin S CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Ctss gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ctss 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 Ctss 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 cathepsin S protein expression.
This CRISPR knockout system enables efficient generation of Ctss-deficient cell models for investigation of cathepsin S signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Ctss exon(s) critical for cathepsin S 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 Ctss genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by cathepsin S CRISPR/Cas9 KO Plasmid (m) and cathepsin S CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ctss locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by cathepsin S HDR Plasmid (m) and cathepsin S HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ctss homology arms to support homology-directed repair at defined Ctss 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.