
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SPUVE CRISPR/Cas9 KO Plasmid (h) | sc-406568 | 20 µg | $397.00 |
PRSS23 encodes the serine protease SPUVE, a trypsin-like enzyme implicated in pericellular proteolysis and remodeling of the extracellular milieu. SPUVE activity has been linked to regulation of epithelial and stromal cell behavior, including migration, adhesion, and differentiation programs that intersect with protease-activated signaling and extracellular matrix dynamics. Expression and functional studies associate PRSS23 with hormone-responsive and inflammatory contexts, suggesting relevance to tissue remodeling and dysregulated growth phenotypes. These properties make PRSS23 a useful target for dissecting protease-dependent pathways that influence cell state transitions and microenvironmental interactions.
SPUVE CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the PRSS23 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the PRSS23 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 PRSS23 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 SPUVE protein expression.
This CRISPR knockout system enables efficient generation of PRSS23-deficient cell models for investigation of SPUVE signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
CRISPRs +/- HDRs
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.