N4BP1 CRISPR/Cas9 KO Plasmid (m): sc-429812
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- N4BP1 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 N4BP1 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 | |
N4BP1 CRISPR/Cas9 KO Plasmid (m) | sc-429812 | 20 µg | $397.00 |
Overview
N4bp1 (N4BP1; NEDD4 binding protein 1) encodes a cytosolic regulator of innate immune signaling that associates with ubiquitin-dependent pathways and modulates inflammatory transcriptional programs. In mouse immune cells, N4BP1 has been linked to control of NF-κB pathway activity downstream of pattern-recognition receptor signaling, influencing cytokine induction and stimulus-dependent activation states. Through its interactions with components of ubiquitination machinery, N4BP1 is positioned to affect signaling complex stability, protein turnover, and downstream transcriptional responses. Dysregulated N4BP1 function is therefore relevant to research on immune homeostasis, infection-driven inflammation, and immune-mediated pathology models.
N4BP1 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the N4bp1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the N4bp1 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 N4bp1 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 N4BP1 protein expression.
This CRISPR knockout system enables efficient generation of N4bp1-deficient cell models for investigation of N4BP1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting N4bp1 exon(s) critical for N4BP1 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 N4bp1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by N4BP1 CRISPR/Cas9 KO Plasmid (m) and N4BP1 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the N4bp1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by N4BP1 HDR Plasmid (m) and N4BP1 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by N4bp1 homology arms to support homology-directed repair at defined N4bp1 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.