Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
NKG2-D CRISPR/Cas9 KO Plasmid (m): sc-424169
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- NKG2-D 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 NKG2-D 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: NKG2-D Antibody (A-7): sc-515599
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
NKG2-D CRISPR/Cas9 KO Plasmid (m) | sc-424169 | 20 µg | $397.00 |
Overview
Klrk1 encodes the activating immunoreceptor NKG2-D (KLRK1), a type II transmembrane C-type lectin–like receptor expressed on mouse NK cells and subsets of CD8+ T cells. NKG2-D recognizes stress-inducible ligands and signals through adaptor proteins to initiate PI3K-, Vav1-, and Syk/ZAP70-linked pathways that promote cytotoxic granule release, cytokine production, and immune surveillance. This axis integrates cues from DNA damage, infection, and cellular transformation to shape innate and adaptive effector responses. Dysregulated NKG2-D–ligand interactions have been implicated in tumor immune evasion, chronic inflammation, and altered control of virally infected or stressed tissues in experimental models.
NKG2-D CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Klrk1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Klrk1 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 Klrk1 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 NKG2-D protein expression.
This CRISPR knockout system enables efficient generation of Klrk1-deficient cell models for investigation of NKG2-D signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Klrk1 exon(s) critical for NKG2-D 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 Klrk1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by NKG2-D CRISPR/Cas9 KO Plasmid (m) and NKG2-D CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Klrk1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by NKG2-D HDR Plasmid (m) and NKG2-D HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Klrk1 homology arms to support homology-directed repair at defined Klrk1 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.