IP3KA CRISPR/Cas9 KO Plasmid (h): sc-404638
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IP3KA 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 IP3KA 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: IP3KA Antibody (F-3): sc-271838
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IP3KA CRISPR/Cas9 KO Plasmid (h) | sc-404638 | 20 µg | $397.00 |
Overview
ITPKA encodes inositol-trisphosphate 3-kinase A (IP3KA), a neuron-enriched enzyme that phosphorylates inositol 1,4,5-trisphosphate (IP3) to generate IP4, thereby reshaping intracellular Ca2+ signaling dynamics. By modulating IP3-dependent calcium release from the endoplasmic reticulum, IP3KA influences synaptic activity, dendritic spine remodeling, and activity-dependent signal transduction. This pathway intersects with phosphoinositide metabolism and calcium-regulated kinase networks that coordinate cytoskeletal organization and transcriptional responses. Dysregulated IP3KA/IP3 signaling has been implicated in altered neuronal plasticity and other signaling phenotypes relevant to neurobiology and cancer-related pathway remodeling.
IP3KA CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the ITPKA gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the ITPKA 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 ITPKA 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 IP3KA protein expression.
This CRISPR knockout system enables efficient generation of ITPKA-deficient cell models for investigation of IP3KA signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting ITPKA exon(s) critical for IP3KA 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 ITPKA genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by IP3KA CRISPR/Cas9 KO Plasmid (h) and IP3KA CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the ITPKA locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by IP3KA HDR Plasmid (h) and IP3KA HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by ITPKA homology arms to support homology-directed repair at defined ITPKA 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.