PIPK I α CRISPR/Cas9 KO Plasmid (m): sc-422243
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PIPK I α 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 PIPK I 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
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: PIPK I α Antibody (D-12): sc-377021
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PIPK I α CRISPR/Cas9 KO Plasmid (m) | sc-422243 | 20 µg | $397.00 |
Overview
Mouse Pip5k1a encodes phosphatidylinositol-4-phosphate 5-kinase type I alpha (PIPK I α), a lipid kinase that generates phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) at the plasma membrane and endomembrane compartments. PI(4,5)P2 supports phosphoinositide-dependent signaling and organizes actin cytoskeletal dynamics, focal adhesion turnover, and membrane trafficking, thereby influencing cell migration, cytokinesis, and receptor-driven signal transduction. Through coupling to PLC-mediated second messenger production and PI3K axis regulation, PIPK I α helps tune pathways controlling proliferation and survival. Dysregulated phosphoinositide metabolism and PI(4,5)P2-dependent cytoskeletal remodeling are implicated in cancer biology, immune cell function, and neurological processes, making Pip5k1a a useful node for mechanistic studies of these phenotypes.
PIPK I α CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Pip5k1a gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Pip5k1a 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 Pip5k1a 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 PIPK I α protein expression.
This CRISPR knockout system enables efficient generation of Pip5k1a-deficient cell models for investigation of PIPK I α signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Pip5k1a exon(s) critical for PIPK I 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 Pip5k1a genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by PIPK I α CRISPR/Cas9 KO Plasmid (m) and PIPK I α CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Pip5k1a locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by PIPK I α HDR Plasmid (m) and PIPK I α HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Pip5k1a homology arms to support homology-directed repair at defined Pip5k1a 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.