NK-2R CRISPR/Cas9 KO Plasmid (h): sc-403149
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- NK-2R 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 NK-2R 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 | |
NK-2R CRISPR/Cas9 KO Plasmid (h) | sc-403149 | 20 µg | $397.00 |
Overview
TACR2 encodes the human neurokinin-2 receptor (NK-2R), a class A GPCR that is activated by tachykinins such as neurokinin A to couple primarily to Gq/11 signaling. Receptor activation stimulates phospholipase Cβ with downstream inositol trisphosphate/diacylglycerol production, intracellular Ca²⁺ mobilization, and PKC/MAPK pathway engagement, shaping transcriptional and contractile programs. NK-2R is expressed in smooth muscle, gastrointestinal and respiratory tissues, and select neuronal populations, where it regulates motility, airway tone, and neurogenic inflammatory signaling. Dysregulated TACR2 signaling has been linked to altered smooth muscle responsiveness and inflammatory circuit modulation, supporting its study in models of asthma-like airway hyperreactivity, gastrointestinal dysmotility, and pain-related neuropeptide pathways.
NK-2R CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TACR2 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TACR2 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 TACR2 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 NK-2R protein expression.
This CRISPR knockout system enables efficient generation of TACR2-deficient cell models for investigation of NK-2R signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting TACR2 exon(s) critical for NK-2R 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 TACR2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by NK-2R CRISPR/Cas9 KO Plasmid (h) and NK-2R CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TACR2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by NK-2R HDR Plasmid (h) and NK-2R HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TACR2 homology arms to support homology-directed repair at defined TACR2 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.