CAR1/2 CRISPR/Cas9 KO Plasmid (m): sc-419458
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CAR1/2 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 CAR1/2 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
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CAR1/2 CRISPR/Cas9 KO Plasmid (m) | sc-419458 | 20 µg | $397.00 |
Overview
Nr1i3 encodes the nuclear receptor constitutive androstane receptor (CAR1/2), a ligand-regulated transcription factor that functions as a central xenobiotic and endobiotic sensor in mouse liver and intestine. Upon activation, CAR forms heterodimers with RXR and binds response elements to regulate Phase I/II metabolizing enzymes and transporters, including cytochrome P450 pathways, glucuronidation, and bile acid handling. CAR signaling intersects with oxidative stress responses, lipid and glucose metabolism, and hepatocyte proliferation programs, shaping adaptive responses to drugs and environmental chemicals. Dysregulated Nr1i3 activity has been linked to altered drug disposition, cholestatic injury susceptibility, and metabolic phenotypes relevant to toxicology and liver disease models.
CAR1/2 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Nr1i3 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Nr1i3 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 Nr1i3 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 CAR1/2 protein expression.
This CRISPR knockout system enables efficient generation of Nr1i3-deficient cell models for investigation of CAR1/2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Nr1i3 exon(s) critical for CAR1/2 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 Nr1i3 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by CAR1/2 CRISPR/Cas9 KO Plasmid (m) and CAR1/2 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Nr1i3 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by CAR1/2 HDR Plasmid (m) and CAR1/2 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Nr1i3 homology arms to support homology-directed repair at defined Nr1i3 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.