Nogo CRISPR/Cas9 KO Plasmid (m): sc-427106
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Nogo 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 Nogo 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: Nogo Antibody (C-4): sc-271878
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Nogo CRISPR/Cas9 KO Plasmid (m) | sc-427106 | 20 µg | $397.00 |
Overview
Rtn4 encodes Nogo, an endoplasmic reticulum–associated reticulon that shapes tubular ER membranes and contributes to organelle homeostasis in neurons and glia. Nogo isoforms also influence neurite outgrowth and synaptic plasticity by modulating cytoskeletal dynamics and signaling pathways linked to axon guidance and regeneration. In the central nervous system, Nogo-mediated inhibition of neurite extension is relevant to mechanisms that limit neuronal remodeling after injury and during neurodegeneration. Mouse Rtn4/Nogo is therefore widely studied in models of axonal growth control, myelination-associated signaling, and stress responses coupled to ER structure.
Nogo CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Rtn4 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Rtn4 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 Rtn4 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 Nogo protein expression.
This CRISPR knockout system enables efficient generation of Rtn4-deficient cell models for investigation of Nogo signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Rtn4 exon(s) critical for Nogo 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 Rtn4 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Nogo CRISPR/Cas9 KO Plasmid (m) and Nogo CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Rtn4 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Nogo HDR Plasmid (m) and Nogo HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Rtn4 homology arms to support homology-directed repair at defined Rtn4 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.