Fgl2 CRISPR/Cas9 KO Plasmid (m): sc-420346
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Fgl2 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 Fgl2 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: Fgl2 Antibody (4H5): sc-100276
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Fgl2 CRISPR/Cas9 KO Plasmid (m) | sc-420346 | 20 µg | $397.00 |
Overview
Fgl2 (fibrinogen-like protein 2) is a membrane-associated and secreted immunoregulatory protein expressed by endothelial cells and myeloid lineages, with roles in hemostasis and inflammatory signaling. In mice, Fgl2 contributes to the prothrombinase activity that links coagulation to innate and adaptive immune responses, influencing cytokine networks and leukocyte recruitment within inflamed tissues. Its expression is modulated downstream of inflammatory cues and has been studied in contexts such as viral hepatitis models, transplant rejection, and tumor-associated immune suppression. These functions make Fgl2 a relevant target for dissecting crosstalk between coagulation pathways, macrophage/T cell regulation, and tissue injury responses.
Fgl2 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Fgl2 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Fgl2 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 Fgl2 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 Fgl2 protein expression.
This CRISPR knockout system enables efficient generation of Fgl2-deficient cell models for investigation of Fgl2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Fgl2 exon(s) critical for Fgl2 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 Fgl2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Fgl2 CRISPR/Cas9 KO Plasmid (m) and Fgl2 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Fgl2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Fgl2 HDR Plasmid (m) and Fgl2 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Fgl2 homology arms to support homology-directed repair at defined Fgl2 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.