ANP CRISPR/Cas9 KO Plasmid (h): sc-400723
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ANP 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 ANP 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: ANP Antibody (F-2): sc-515701
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ANP CRISPR/Cas9 KO Plasmid (h) | sc-400723 | 20 µg | $397.00 |
Overview
NPPA encodes atrial natriuretic peptide (ANP), a cardiac-derived hormone that regulates blood volume and vascular tone through natriuretic peptide receptors and downstream cGMP/PKG signaling. ANP promotes natriuresis, diuresis, and vasodilation, and modulates renin–angiotensin–aldosterone axis activity, linking myocardial stretch sensing to systemic fluid–electrolyte homeostasis. NPPA expression is tightly controlled in cardiomyocytes and is dynamically induced during cardiac stress remodeling. Dysregulated NPPA/ANP signaling is associated with cardiovascular pathophysiology, including hypertension, cardiac hypertrophy, and heart failure, making it a key node for mechanistic studies of cardiometabolic and hemodynamic regulation.
ANP CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the NPPA gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the NPPA 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 NPPA 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 ANP protein expression.
This CRISPR knockout system enables efficient generation of NPPA-deficient cell models for investigation of ANP signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting NPPA exon(s) critical for ANP 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 NPPA genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ANP CRISPR/Cas9 KO Plasmid (h) and ANP CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the NPPA locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ANP HDR Plasmid (h) and ANP HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by NPPA homology arms to support homology-directed repair at defined NPPA 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.