NIK CRISPR/Cas9 KO Plasmid (m): sc-424749
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- NIK 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 NIK 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: NIK Antibody (A-12): sc-8417
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
NIK CRISPR/Cas9 KO Plasmid (m) | sc-424749 | 20 µg | $397.00 |
Overview
Map3k14 encodes NF-κB–inducing kinase (NIK), a MAP3K that serves as a central regulator of the noncanonical NF-κB pathway in mouse cells. NIK integrates signals from select TNF receptor superfamily members to promote processing of NF-κB2 p100 to p52 via IKKα, thereby shaping transcriptional programs that control lymphoid organogenesis, B-cell maturation, dendritic cell function, and inflammatory cytokine networks. Tight control of NIK stability is critical for immune homeostasis, and dysregulated NIK signaling has been linked to chronic inflammation, immune dysregulation, and oncogenic processes in lymphoid and stromal compartments. As a signaling node upstream of NF-κB2/RelB, NIK is frequently studied in contexts such as autoimmune-like phenotypes, infection-driven immune remodeling, and tumor-associated inflammatory microenvironments.
NIK CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Map3k14 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Map3k14 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 Map3k14 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 NIK protein expression.
This CRISPR knockout system enables efficient generation of Map3k14-deficient cell models for investigation of NIK signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Map3k14 exon(s) critical for NIK 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 Map3k14 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by NIK CRISPR/Cas9 KO Plasmid (m) and NIK CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Map3k14 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by NIK HDR Plasmid (m) and NIK HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Map3k14 homology arms to support homology-directed repair at defined Map3k14 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.