BNP CRISPR/Cas9 KO Plasmid (m): sc-421946
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BNP CRISPR/Cas9 Knockout (KO) Plasmid (m) 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 BNP 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 | |
BNP CRISPR/Cas9 KO Plasmid (m) | sc-421946 | 20 µg | $397.00 |
Overview
Nppb encodes B-type natriuretic peptide (BNP), a secreted cardiac hormone upregulated by myocardial stretch and neurohormonal cues. After processing from proBNP, BNP signals through natriuretic peptide receptors to stimulate guanylyl cyclase activity, elevate cGMP, and modulate vascular tone, natriuresis, and cardiac remodeling programs. In mice, Nppb expression is widely used as a molecular readout of hemodynamic stress and cardiomyocyte hypertrophy, linking it to pathways controlling fibrosis, extracellular matrix turnover, and inflammatory signaling. Dysregulated BNP/NP signaling is relevant to studies of cardiac pressure overload, heart failure–associated remodeling phenotypes, and cardio-renal homeostasis.
BNP CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Nppb gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Nppb 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 Nppb 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 BNP protein expression.
This CRISPR knockout system enables efficient generation of Nppb-deficient cell models for investigation of BNP signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Nppb exon(s) critical for BNP 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 Nppb genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by BNP CRISPR/Cas9 KO Plasmid (m) and BNP CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Nppb locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by BNP HDR Plasmid (m) and BNP HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Nppb homology arms to support homology-directed repair at defined Nppb 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.