Ninjurin-1 CRISPR/Cas9 KO Plasmid (m): sc-421898
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Ninjurin-1 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 Ninjurin-1 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: Ninjurin-1 Antibody (50): sc-136295
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Ninjurin-1 CRISPR/Cas9 KO Plasmid (m) | sc-421898 | 20 µg | $397.00 |
Overview
Ninj1 encodes Ninjurin-1, a cell-surface adhesion molecule induced by nerve injury that modulates cell–cell interactions and communication between neurons, glia, and infiltrating immune cells. Ninjurin-1 participates in processes linked to axonal regeneration, leukocyte trafficking, and inflammatory signaling, with reported connections to NF-κB–associated responses and myeloid cell activation. In mouse systems, Ninj1 expression is frequently studied in the context of tissue damage, neuroinflammation, and macrophage-mediated remodeling, where altered regulation can influence injury responses. These properties make Ninjurin-1 a useful node for dissecting how adhesion and inflammation intersect in nervous system and peripheral tissue pathophysiology.
Ninjurin-1 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Ninj1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ninj1 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 Ninj1 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 Ninjurin-1 protein expression.
This CRISPR knockout system enables efficient generation of Ninj1-deficient cell models for investigation of Ninjurin-1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Ninj1 exon(s) critical for Ninjurin-1 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 Ninj1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Ninjurin-1 CRISPR/Cas9 KO Plasmid (m) and Ninjurin-1 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ninj1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Ninjurin-1 HDR Plasmid (m) and Ninjurin-1 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ninj1 homology arms to support homology-directed repair at defined Ninj1 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.