pki γ CRISPR/Cas9 KO Plasmid (h): sc-411573
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- pki γ 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 pki γ 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: pki γ Antibody (D-8): sc-515108
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
pki γ CRISPR/Cas9 KO Plasmid (h) | sc-411573 | 20 µg | $397.00 |
Overview
PKIG encodes protein kinase inhibitor gamma (PKIγ), an endogenous inhibitor of cAMP-dependent protein kinase A (PKA) that helps constrain basal and stimulus-induced PKA signaling. By binding the catalytic subunit of PKA, PKIγ modulates phosphorylation-dependent control of transcription, metabolism, cell-cycle progression, and cytoskeletal dynamics downstream of GPCR–adenylyl cyclase–cAMP pathways. PKIG activity intersects with CREB-regulated gene expression and broader kinase signaling networks that shape cellular stress responses and differentiation programs. Dysregulated cAMP/PKA signaling has been implicated across multiple disease-relevant processes, including tumor cell growth, endocrine signaling abnormalities, and neuronal function, making PKIG a useful node for mechanistic studies.
pki γ CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the PKIG gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the PKIG 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 PKIG 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 pki γ protein expression.
This CRISPR knockout system enables efficient generation of PKIG-deficient cell models for investigation of pki γ signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting PKIG exon(s) critical for pki γ 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 PKIG genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by pki γ CRISPR/Cas9 KO Plasmid (h) and pki γ CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the PKIG locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by pki γ HDR Plasmid (h) and pki γ HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by PKIG homology arms to support homology-directed repair at defined PKIG 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.