HCII CRISPR/Cas9 KO Plasmid (m): sc-420808
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- HCII 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 HCII 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 | |
HCII CRISPR/Cas9 KO Plasmid (m) | sc-420808 | 20 µg | $397.00 |
Overview
Serpind1 encodes heparin cofactor II (HCII), a serine protease inhibitor that selectively inactivates thrombin, with activity markedly enhanced by glycosaminoglycans such as dermatan sulfate. By constraining thrombin proteolysis, HCII modulates coagulation and interfaces with thrombin-driven signaling pathways that influence platelet activation, vascular inflammation, and extracellular matrix remodeling. In mouse systems, Serpind1 function is commonly examined in the context of hemostasis and vascular biology, where altered thrombin control can affect thrombosis-related phenotypes and inflammatory responses. Dysregulation of serpin–protease balance is relevant to models of thrombo-inflammatory disease mechanisms and vascular injury responses.
HCII CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Serpind1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Serpind1 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 Serpind1 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 HCII protein expression.
This CRISPR knockout system enables efficient generation of Serpind1-deficient cell models for investigation of HCII signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Serpind1 exon(s) critical for HCII 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 Serpind1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by HCII CRISPR/Cas9 KO Plasmid (m) and HCII CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Serpind1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by HCII HDR Plasmid (m) and HCII HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Serpind1 homology arms to support homology-directed repair at defined Serpind1 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.