KIR2.1 CRISPR/Cas9 KO Plasmid (h): sc-401974
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- KIR2.1 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 KIR2.1 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 | |
KIR2.1 CRISPR/Cas9 KO Plasmid (h) | sc-401974 | 20 µg | $397.00 |
Overview
KCNJ2 encodes the human inwardly rectifying potassium channel Kir2.1, a key determinant of the cardiac and skeletal muscle resting membrane potential and excitability. Kir2.1 conducts IK1 currents that stabilize terminal repolarization and shape action potential waveforms, integrating with membrane trafficking and PIP2-dependent gating processes. Altered KCNJ2 function is linked to channelopathy phenotypes such as Andersen–Tawil syndrome and can influence arrhythmia susceptibility, periodic paralysis, and developmental signaling in excitable tissues. In cell models, Kir2.1 activity intersects with electrophysiological homeostasis, calcium handling, and membrane potential–dependent regulation of gene expression.
KIR2.1 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the KCNJ2 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the KCNJ2 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 KCNJ2 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 KIR2.1 protein expression.
This CRISPR knockout system enables efficient generation of KCNJ2-deficient cell models for investigation of KIR2.1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting KCNJ2 exon(s) critical for KIR2.1 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 KCNJ2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by KIR2.1 CRISPR/Cas9 KO Plasmid (h) and KIR2.1 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the KCNJ2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by KIR2.1 HDR Plasmid (h) and KIR2.1 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by KCNJ2 homology arms to support homology-directed repair at defined KCNJ2 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.