KLK12 CRISPR/Cas9 KO Plasmid (h): sc-407376
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- KLK12 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 KLK12 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 | |
KLK12 CRISPR/Cas9 KO Plasmid (h) | sc-407376 | 20 µg | $397.00 |
Overview
KLK12 encodes kallikrein-related peptidase 12, a secreted serine protease that contributes to extracellular matrix remodeling and pericellular proteolysis. By processing peptide substrates and influencing protease cascade activity, KLK12 can modulate cell–matrix interactions, tissue homeostasis, and signaling events linked to migration and angiogenic responses. Altered KLK12 expression has been reported in multiple human pathologies, including cancers, where changes in proteolytic balance can affect invasion-associated microenvironmental processes. As a soluble protease with context-dependent activity, KLK12 is often studied in models of tumor biology, vascular regulation, and inflammation-related tissue remodeling.
KLK12 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the KLK12 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the KLK12 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 KLK12 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 KLK12 protein expression.
This CRISPR knockout system enables efficient generation of KLK12-deficient cell models for investigation of KLK12 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting KLK12 exon(s) critical for KLK12 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 KLK12 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by KLK12 CRISPR/Cas9 KO Plasmid (h) and KLK12 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the KLK12 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by KLK12 HDR Plasmid (h) and KLK12 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by KLK12 homology arms to support homology-directed repair at defined KLK12 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.