NFκB p50 CRISPR/Cas9 KO Plasmid (m): sc-421876
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- NFκB p50 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 NFκB p50 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: p-NFκB p50 Antibody (A-8): sc-271908
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
NFκB p50 CRISPR/Cas9 KO Plasmid (m) | sc-421876 | 20 µg | $397.00 |
Overview
Nfkb1 encodes NFκB p50, a core DNA-binding component of the NF-κB transcription factor family generated by processing of the p105 precursor. NFκB p50 participates in canonical NF-κB signaling downstream of receptors such as TNFR, IL-1R, and Toll-like receptors to regulate inflammatory gene expression, innate and adaptive immune responses, cell survival, and stress signaling. Depending on dimer composition, p50-containing complexes can activate transcription (e.g., with RelA/p65) or repress it (e.g., p50 homodimers), shaping cytokine programs and macrophage and lymphocyte function. Dysregulation of Nfkb1-driven pathways is widely used as a mechanistic link in mouse models of chronic inflammation, autoimmunity, infection, and tumor-promoting inflammatory microenvironments.
NFκB p50 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Nfkb1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Nfkb1 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 Nfkb1 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 NFκB p50 protein expression.
This CRISPR knockout system enables efficient generation of Nfkb1-deficient cell models for investigation of NFκB p50 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Nfkb1 exon(s) critical for NFκB p50 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 Nfkb1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by NFκB p50 CRISPR/Cas9 KO Plasmid (m) and NFκB p50 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Nfkb1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by NFκB p50 HDR Plasmid (m) and NFκB p50 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Nfkb1 homology arms to support homology-directed repair at defined Nfkb1 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.