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.
Rrn3 CRISPR/Cas9 KO Plasmid (h): sc-403709
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Rrn3 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 Rrn3 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: Rrn3 Antibody (D-9): sc-390464
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Rrn3 CRISPR/Cas9 KO Plasmid (h) | sc-403709 | 20 µg | $397.00 |
Overview
RRN3 encodes Rrn3, a Pol I–associated transcription factor that helps recruit RNA polymerase I to ribosomal DNA and supports pre-rRNA synthesis, linking growth cues to ribosome biogenesis. Rrn3 activity is regulated by nutrient and stress-responsive signaling, including mTOR-dependent control of Pol I initiation, and it contributes to nucleolar function and proteostasis by governing rRNA output. Because rDNA transcription is tightly coupled to proliferation and cellular stress adaptation, altered RRN3–Pol I dynamics are studied in contexts of dysregulated growth, genomic instability, and nucleolar stress phenotypes. RRN3 is therefore relevant for investigating how ribosome biogenesis interfaces with cell cycle control and metabolic reprogramming.
Rrn3 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the RRN3 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the RRN3 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 RRN3 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 Rrn3 protein expression.
This CRISPR knockout system enables efficient generation of RRN3-deficient cell models for investigation of Rrn3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting RRN3 exon(s) critical for Rrn3 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 RRN3 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Rrn3 CRISPR/Cas9 KO Plasmid (h) and Rrn3 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the RRN3 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Rrn3 HDR Plasmid (h) and Rrn3 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by RRN3 homology arms to support homology-directed repair at defined RRN3 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.