ATP7A CRISPR/Cas9 KO Plasmid (m): sc-419259
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ATP7A 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 ATP7A 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 | |
ATP7A CRISPR/Cas9 KO Plasmid (m) | sc-419259 | 20 µg | $397.00 |
Overview
Atp7a encodes ATP7A, a P-type ATPase copper transporter that regulates intracellular copper distribution by shuttling between the trans-Golgi network and plasma membrane in response to copper levels. By delivering copper to secretory pathway enzymes and promoting copper efflux, ATP7A supports copper-dependent processes including oxidative stress control, extracellular matrix crosslinking, and iron homeostasis via cuproenzyme maturation. ATP7A activity intersects with vesicular trafficking, metal ion homeostasis, and redox signaling pathways, and its dysfunction perturbs systemic and cellular copper balance. In mouse models, altered Atp7a function is used to study mechanisms of copper-dependent neurodevelopmental and connective tissue phenotypes and broader metabolic stress responses.
ATP7A CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Atp7a gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Atp7a 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 Atp7a 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 ATP7A protein expression.
This CRISPR knockout system enables efficient generation of Atp7a-deficient cell models for investigation of ATP7A signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Atp7a exon(s) critical for ATP7A 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 Atp7a genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ATP7A CRISPR/Cas9 KO Plasmid (m) and ATP7A CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Atp7a locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ATP7A HDR Plasmid (m) and ATP7A HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Atp7a homology arms to support homology-directed repair at defined Atp7a 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.