PI 4-kinase α CRISPR/Cas9 KO Plasmid (h): sc-406508
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PI 4-kinase α 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 PI 4-kinase α 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 | |
PI 4-kinase α CRISPR/Cas9 KO Plasmid (h) | sc-406508 | 20 µg | $397.00 |
Overview
PI4KA encodes phosphatidylinositol 4-kinase alpha (PI 4-kinase α), a lipid kinase that generates phosphatidylinositol 4-phosphate (PI4P), a key precursor for phosphoinositides that organize membrane identity and signaling. PI 4-kinase α supports Golgi and plasma membrane PI4P pools, influencing vesicular trafficking, phosphoinositide-dependent signal transduction, and cytoskeletal dynamics. Through its impact on membrane lipid homeostasis, PI4KA is relevant to studies of cellular stress responses and remodeling of endomembrane compartments, and altered phosphoinositide metabolism has been associated with diverse human disease mechanisms including neurodevelopmental and oncogenic processes.
PI 4-kinase α CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the PI4KA gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the PI4KA 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 PI4KA 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 PI 4-kinase α protein expression.
This CRISPR knockout system enables efficient generation of PI4KA-deficient cell models for investigation of PI 4-kinase α signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting PI4KA exon(s) critical for PI 4-kinase α 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 PI4KA genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by PI 4-kinase α CRISPR/Cas9 KO Plasmid (h) and PI 4-kinase α CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the PI4KA locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by PI 4-kinase α HDR Plasmid (h) and PI 4-kinase α HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by PI4KA homology arms to support homology-directed repair at defined PI4KA 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.