TFPI-2 CRISPR/Cas9 KO Plasmid (m): sc-423362
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TFPI-2 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 TFPI-2 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 | |
TFPI-2 CRISPR/Cas9 KO Plasmid (m) | sc-423362 | 20 µg | $397.00 |
Overview
Tfpi2 encodes tissue factor pathway inhibitor 2 (TFPI-2), a secreted Kunitz-type serine protease inhibitor that modulates extracellular proteolysis by inhibiting proteases such as plasmin and trypsin-like enzymes. In mouse tissues, TFPI-2 helps regulate extracellular matrix turnover, pericellular protease activity, and cell–matrix interactions that influence adhesion, migration, and tissue remodeling. By constraining proteolytic cascades linked to coagulation and fibrinolysis and interfacing with matrix metalloproteinase-driven remodeling, TFPI-2 contributes to vascular and stromal homeostasis. Altered TFPI-2 expression or activity has been associated with dysregulated matrix degradation and invasive cellular phenotypes relevant to fibrosis, vascular pathology, and cancer biology.
TFPI-2 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Tfpi2 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Tfpi2 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 Tfpi2 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 TFPI-2 protein expression.
This CRISPR knockout system enables efficient generation of Tfpi2-deficient cell models for investigation of TFPI-2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Tfpi2 exon(s) critical for TFPI-2 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 Tfpi2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TFPI-2 CRISPR/Cas9 KO Plasmid (m) and TFPI-2 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Tfpi2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TFPI-2 HDR Plasmid (m) and TFPI-2 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Tfpi2 homology arms to support homology-directed repair at defined Tfpi2 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.