NAT-3 CRISPR/Cas9 KO Plasmid (m): sc-421825
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- NAT-3 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 NAT-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 | |
NAT-3 CRISPR/Cas9 KO Plasmid (m) | sc-421825 | 20 µg | $397.00 |
Overview
Mouse Nat3 encodes NAT-3, a member of the arylamine N-acetyltransferase family that catalyzes acetyl-CoA–dependent N-acetylation reactions involved in xenobiotic biotransformation. NAT-3 contributes to cellular detoxification capacity by modulating the chemical reactivity and clearance of aromatic amines and related compounds, intersecting with hepatic and extrahepatic metabolic processes. Variation in NAT enzyme activity is broadly relevant to chemical susceptibility and toxicant-driven tissue responses, supporting the use of Nat3 models in studies of metabolism-associated stress and inflammation. In mice, Nat3 loss-of-function can help clarify how acetylation-dependent metabolism influences downstream cellular homeostasis under defined exposure conditions.
NAT-3 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Nat3 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Nat3 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 Nat3 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 NAT-3 protein expression.
This CRISPR knockout system enables efficient generation of Nat3-deficient cell models for investigation of NAT-3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Nat3 exon(s) critical for NAT-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 Nat3 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by NAT-3 CRISPR/Cas9 KO Plasmid (m) and NAT-3 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Nat3 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by NAT-3 HDR Plasmid (m) and NAT-3 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Nat3 homology arms to support homology-directed repair at defined Nat3 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.