ATP8A1 CRISPR/Cas9 KO Plasmid (h): sc-406843
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ATP8A1 CRISPR/Cas9 Knockout (KO) Plasmid (h) 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 ATP8A1 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 | |
ATP8A1 CRISPR/Cas9 KO Plasmid (h) | sc-406843 | 20 µg | $397.00 |
Overview
ATP8A1 encodes a P4-ATPase phospholipid flippase that maintains plasma membrane lipid asymmetry by translocating aminophospholipids such as phosphatidylserine and phosphatidylethanolamine between membrane leaflets. Through this activity, ATP8A1 supports membrane curvature, vesicle budding, and endocytic trafficking, influencing cytoskeletal organization and polarized membrane dynamics. Disruption of lipid asymmetry can alter signaling platforms and membrane-dependent processes, linking ATP8A1 function to pathways governing intracellular transport and cell survival. ATP8A1 dysregulation has been investigated in the context of neurological and metabolic phenotypes where membrane composition and trafficking are critical determinants of cellular homeostasis.
ATP8A1 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the ATP8A1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the ATP8A1 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 ATP8A1 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 ATP8A1 protein expression.
This CRISPR knockout system enables efficient generation of ATP8A1-deficient cell models for investigation of ATP8A1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting ATP8A1 exon(s) critical for ATP8A1 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 ATP8A1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ATP8A1 CRISPR/Cas9 KO Plasmid (h) and ATP8A1 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the ATP8A1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ATP8A1 HDR Plasmid (h) and ATP8A1 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by ATP8A1 homology arms to support homology-directed repair at defined ATP8A1 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.