Date published: 2026-7-10

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RD3 CRISPR/Cas9 KO Plasmid (h): sc-405841

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • RD3 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 RD3 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: RD3 Antibody (A-9): sc-390653
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    RD3 CRISPR/Cas9 KO Plasmid (h)

    sc-405841
    20 µg
    $397.00

    Overview

    RD3 (retinal degeneration 3) encodes a small cytosolic protein that is highly enriched in photoreceptors and supports normal phototransduction homeostasis. RD3 regulates the trafficking and stability of retinal guanylate cyclases (e.g., GUCY2D/GC-E), influencing cGMP synthesis and downstream signaling that controls ion channel activity in outer segments. Through these interactions, RD3 contributes to ciliary/outer segment protein targeting and protection of guanylate cyclases from inappropriate activation. Disruption of RD3 function is associated with inherited retinal degenerations, making it a useful target for dissecting mechanisms of photoreceptor maintenance and cGMP-dependent signaling.

    RD3 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the RD3 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the RD3 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 RD3 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 RD3 protein expression.

    This CRISPR knockout system enables efficient generation of RD3-deficient cell models for investigation of RD3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting RD3 exon(s) critical for RD3 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 RD3 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by RD3 CRISPR/Cas9 KO Plasmid (h) and RD3 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the RD3 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by RD3 HDR Plasmid (h) and RD3 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by RD3 homology arms to support homology-directed repair at defined RD3 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.