RENBP CRISPR/Cas9 KO Plasmid (m): sc-422648
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RENBP 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 RENBP 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 | |
RENBP CRISPR/Cas9 KO Plasmid (m) | sc-422648 | 20 µg | $397.00 |
Overview
Renbp encodes renin binding protein (RENBP), a membrane-associated protein implicated in regulating components of the renin–angiotensin system and related proteolytic processing pathways. In mouse tissues, RENBP expression has been linked to modulation of renin availability and downstream signaling that influences vascular tone, electrolyte homeostasis, and inflammatory responses. Through these connections, Renbp is relevant for mechanistic studies of blood pressure regulation and cardiometabolic stress pathways. Altered renin–angiotensin signaling is also associated with renal and cardiovascular pathology, making Renbp a useful node for interrogating gene networks that couple protease regulation to systemic physiology.
RENBP CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Renbp gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Renbp 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 Renbp 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 RENBP protein expression.
This CRISPR knockout system enables efficient generation of Renbp-deficient cell models for investigation of RENBP signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Renbp exon(s) critical for RENBP 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 Renbp genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by RENBP CRISPR/Cas9 KO Plasmid (m) and RENBP CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Renbp locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by RENBP HDR Plasmid (m) and RENBP HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Renbp homology arms to support homology-directed repair at defined Renbp 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.