ILT-3 CRISPR/Cas9 KO Plasmid (h): sc-407764
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ILT-3 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 ILT-3 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 | |
ILT-3 CRISPR/Cas9 KO Plasmid (h) | sc-407764 | 20 µg | $397.00 |
Overview
LILRB4 encodes immunoglobulin-like transcript 3 (ILT-3), an inhibitory leukocyte receptor predominantly expressed on myeloid antigen-presenting cells such as dendritic cells and monocytes/macrophages. ILT-3 contributes to immune homeostasis by transducing inhibitory signals via ITIM-dependent recruitment of phosphatases, dampening activating pathways linked to antigen presentation, costimulation, and inflammatory cytokine production. Through these mechanisms, ILT-3 helps shape T cell polarization and tolerance-associated programs within myeloid–lymphoid crosstalk. Dysregulated LILRB4/ILT-3 expression has been studied in contexts of chronic inflammation, immune evasion in the tumor microenvironment, and myeloid lineage malignancies, where altered inhibitory signaling can modulate immune surveillance and tissue immunity.
ILT-3 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the LILRB4 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the LILRB4 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 LILRB4 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 ILT-3 protein expression.
This CRISPR knockout system enables efficient generation of LILRB4-deficient cell models for investigation of ILT-3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting LILRB4 exon(s) critical for ILT-3 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 LILRB4 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ILT-3 CRISPR/Cas9 KO Plasmid (h) and ILT-3 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the LILRB4 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ILT-3 HDR Plasmid (h) and ILT-3 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by LILRB4 homology arms to support homology-directed repair at defined LILRB4 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.