CNP-53 CRISPR/Cas9 KO Plasmid (h): sc-403527
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CNP-53 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 CNP-53 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: CNP Antibody (C-9): sc-374043
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CNP-53 CRISPR/Cas9 KO Plasmid (h) | sc-403527 | 20 µg | $397.00 |
Overview
NPPC encodes C-type natriuretic peptide, and the CNP-53 isoform is a bioactive secreted peptide that signals primarily through natriuretic peptide receptor 2 (NPR2/guanylyl cyclase B) to elevate intracellular cGMP. This pathway regulates endochondral ossification and cartilage homeostasis, modulates vascular tone and endothelial function, and influences fibroblast activity and extracellular matrix remodeling. CNP/NPR2 signaling intersects with MAPK and nitric oxide–cGMP networks, shaping proliferative and differentiation programs in mesenchymal and vascular cell types. Dysregulated NPPC activity has been associated with growth plate and skeletal development phenotypes, as well as cardiometabolic and fibrotic processes relevant to disease modeling.
CNP-53 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the NPPC gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the NPPC 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 NPPC 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 CNP-53 protein expression.
This CRISPR knockout system enables efficient generation of NPPC-deficient cell models for investigation of CNP-53 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting NPPC exon(s) critical for CNP-53 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 NPPC genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by CNP-53 CRISPR/Cas9 KO Plasmid (h) and CNP-53 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the NPPC locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by CNP-53 HDR Plasmid (h) and CNP-53 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by NPPC homology arms to support homology-directed repair at defined NPPC 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.