Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
p53R2 CRISPR/Cas9 KO Plasmid (h): sc-402192
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- p53R2 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 p53R2 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: p53R2 Antibody (H-3): sc-137173
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
p53R2 CRISPR/Cas9 KO Plasmid (h) | sc-402192 | 20 µg | $397.00 |
Overview
RRM2B encodes p53R2, a p53-inducible small subunit of ribonucleotide reductase that supplies deoxyribonucleotides for DNA synthesis and repair, particularly under stress conditions. p53R2 supports mitochondrial DNA maintenance and contributes to redox balance and cell survival during replication stress by sustaining dNTP pools. Functionally, it links the DNA damage response, p53 signaling, and nucleotide metabolism, influencing genome stability and checkpoint control. Dysregulation of RRM2B has been associated with mitochondrial DNA depletion phenotypes and cancer-related stress adaptation, making it relevant for studies of genomic maintenance and metabolic rewiring.
p53R2 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the RRM2B gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the RRM2B 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 RRM2B 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 p53R2 protein expression.
This CRISPR knockout system enables efficient generation of RRM2B-deficient cell models for investigation of p53R2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting RRM2B exon(s) critical for p53R2 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 RRM2B genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by p53R2 CRISPR/Cas9 KO Plasmid (h) and p53R2 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the RRM2B locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by p53R2 HDR Plasmid (h) and p53R2 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by RRM2B homology arms to support homology-directed repair at defined RRM2B 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.