RPGR CRISPR/Cas9 KO Plasmid (h): sc-404441
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RPGR 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 RPGR 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 | |
RPGR CRISPR/Cas9 KO Plasmid (h) | sc-404441 | 20 µg | $397.00 |
Overview
RPGR (retinitis pigmentosa GTPase regulator) encodes a ciliary protein enriched at the connecting cilium of photoreceptors, where it supports intraflagellar transport and trafficking of membrane-associated cargos required for outer segment maintenance. RPGR interacts with cilia-associated complexes and contributes to microtubule-based transport processes that preserve cilium structure and signaling competence. Disruption of RPGR perturbs ciliary function and photoreceptor homeostasis, linking its loss of function to inherited retinal degeneration phenotypes such as X-linked retinitis pigmentosa. In biomedical research, RPGR is commonly studied in the context of ciliopathy mechanisms, photoreceptor cell biology, and genotype–phenotype relationships in retinal disease.
RPGR CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the RPGR gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the RPGR 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 RPGR 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 RPGR protein expression.
This CRISPR knockout system enables efficient generation of RPGR-deficient cell models for investigation of RPGR signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting RPGR exon(s) critical for RPGR 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 RPGR genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by RPGR CRISPR/Cas9 KO Plasmid (h) and RPGR CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the RPGR locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by RPGR HDR Plasmid (h) and RPGR HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by RPGR homology arms to support homology-directed repair at defined RPGR 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.