CLEC-2D CRISPR/Cas9 KO Plasmid (h): sc-412035
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CLEC-2D CRISPR/Cas9 Knockout (KO) Plasmid (h) 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 CLEC-2D 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 | |
CLEC-2D CRISPR/Cas9 KO Plasmid (h) | sc-412035 | 20 µg | $397.00 |
Overview
CLEC2D encodes CLEC-2D, a type II transmembrane C-type lectin–like ligand that modulates immune surveillance by engaging the inhibitory receptor KLRB1/CD161 on NK cells and subsets of T cells. Through this axis, CLEC-2D can shape cytotoxic effector function, cytokine production, and cell–cell communication at immune–tissue interfaces. Expression of CLEC2D is dynamically regulated by cellular stress and differentiation states, linking it to pathways governing immune evasion, inflammation, and tumor–immune interactions. Dysregulated CLEC2D signaling has been reported in multiple malignancies and inflammatory contexts, supporting its use as a mechanistic node for studying NK/T-cell regulation in human systems.
CLEC-2D CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the CLEC2D gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the CLEC2D 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 CLEC2D 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 CLEC-2D protein expression.
This CRISPR knockout system enables efficient generation of CLEC2D-deficient cell models for investigation of CLEC-2D signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting CLEC2D exon(s) critical for CLEC-2D 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 CLEC2D genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by CLEC-2D CRISPR/Cas9 KO Plasmid (h) and CLEC-2D CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the CLEC2D locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by CLEC-2D HDR Plasmid (h) and CLEC-2D HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by CLEC2D homology arms to support homology-directed repair at defined CLEC2D 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.