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.
B7-2 CRISPR/Cas9 KO Plasmid (m): sc-419575
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- B7-2 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 B7-2 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: B7-2 Antibody (D-6): sc-28347
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
B7-2 CRISPR/Cas9 KO Plasmid (m) | sc-419575 | 20 µg | $397.00 |
Overview
Cd86 encodes the co-stimulatory ligand B7-2 (CD86), a type I transmembrane glycoprotein expressed on antigen-presenting cells such as dendritic cells, macrophages, and B cells. B7-2 engages CD28 and CTLA-4 on T cells to tune activation thresholds, cytokine production, and peripheral tolerance, integrating with TCR signaling, NF-κB/AP-1 transcriptional programs, and immune checkpoint regulation. Its inducible expression during innate immune sensing links inflammatory cues to adaptive immune priming and germinal center responses. Dysregulated CD86 activity is implicated in models of autoimmunity, chronic inflammation, transplantation responses, and tumor immune evasion, making it a key node for immunology and immuno-oncology research.
B7-2 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Cd86 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Cd86 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 Cd86 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 B7-2 protein expression.
This CRISPR knockout system enables efficient generation of Cd86-deficient cell models for investigation of B7-2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Cd86 exon(s) critical for B7-2 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 Cd86 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by B7-2 CRISPR/Cas9 KO Plasmid (m) and B7-2 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Cd86 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by B7-2 HDR Plasmid (m) and B7-2 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Cd86 homology arms to support homology-directed repair at defined Cd86 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.