BTN2A2 CRISPR/Cas9 KO Plasmid (m): sc-433634
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BTN2A2 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 BTN2A2 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 | |
BTN2A2 CRISPR/Cas9 KO Plasmid (m) | sc-433634 | 20 µg | $397.00 |
Overview
Btn2a2 encodes butyrophilin subfamily 2 member A2 (BTN2A2), an immunoglobulin superfamily transmembrane protein that functions as a co-inhibitory regulator of T cell responses. In mice, BTN2A2 expression on antigen-presenting cells modulates T cell activation thresholds, supporting peripheral tolerance by limiting proliferation and cytokine production. This checkpoint-like activity places BTN2A2 within pathways governing immune synapse signaling, costimulation, and maintenance of immune homeostasis. Dysregulated BTN2A2 signaling has been linked to altered inflammatory responses relevant to autoimmunity, infection, and tumor-immune interactions in experimental models.
BTN2A2 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Btn2a2 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Btn2a2 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 Btn2a2 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 BTN2A2 protein expression.
This CRISPR knockout system enables efficient generation of Btn2a2-deficient cell models for investigation of BTN2A2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Btn2a2 exon(s) critical for BTN2A2 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 Btn2a2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by BTN2A2 CRISPR/Cas9 KO Plasmid (m) and BTN2A2 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Btn2a2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by BTN2A2 HDR Plasmid (m) and BTN2A2 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Btn2a2 homology arms to support homology-directed repair at defined Btn2a2 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.