ATP13A3 CRISPR/Cas9 KO Plasmid (h): sc-413173
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ATP13A3 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 ATP13A3 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 | |
ATP13A3 CRISPR/Cas9 KO Plasmid (h) | sc-413173 | 20 µg | $397.00 |
Overview
ATP13A3 encodes a P5-type ATPase implicated in cation homeostasis and membrane trafficking within the endolysosomal system, contributing to regulation of vesicular transport and intracellular compartment integrity. By influencing ion gradients and organelle function, ATP13A3 can affect cellular stress responses, metabolic adaptation, and signaling processes linked to membrane dynamics. Altered ATP13A3 activity has been associated with cardiovascular and pulmonary vascular biology, including genetic links reported in pulmonary arterial hypertension, supporting its relevance to studies of vascular remodeling and endothelial cell function. Its expression and proposed role in maintaining cellular homeostasis also make it pertinent for investigating mechanisms of proliferation, survival, and transport-dependent signaling.
ATP13A3 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the ATP13A3 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the ATP13A3 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 ATP13A3 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 ATP13A3 protein expression.
This CRISPR knockout system enables efficient generation of ATP13A3-deficient cell models for investigation of ATP13A3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting ATP13A3 exon(s) critical for ATP13A3 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 ATP13A3 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ATP13A3 CRISPR/Cas9 KO Plasmid (h) and ATP13A3 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the ATP13A3 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ATP13A3 HDR Plasmid (h) and ATP13A3 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by ATP13A3 homology arms to support homology-directed repair at defined ATP13A3 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.