RSP3 CRISPR/Cas9 KO Plasmid (h): sc-413513
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RSP3 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 RSP3 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 | |
RSP3 CRISPR/Cas9 KO Plasmid (h) | sc-413513 | 20 µg | $397.00 |
Overview
RSPH3 encodes radial spoke head 3 homolog (RSP3), a structural component of the radial spoke complex in motile cilia and flagella that helps couple axonemal dynein activity to coordinated microtubule sliding and ciliary beat regulation. Through its role within the 9+2 axoneme architecture, RSP3 supports proper waveform generation and efficient mucociliary clearance. Disruption of radial spoke assembly or signaling is linked to motile ciliopathies, including primary ciliary dyskinesia phenotypes characterized by impaired ciliary motility. As a result, RSPH3 is widely studied in pathways governing cilia biogenesis, axonemal organization, and respiratory reproductive tract physiology.
RSP3 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the RSPH3 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the RSPH3 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 RSPH3 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 RSP3 protein expression.
This CRISPR knockout system enables efficient generation of RSPH3-deficient cell models for investigation of RSP3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting RSPH3 exon(s) critical for RSP3 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 RSPH3 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by RSP3 CRISPR/Cas9 KO Plasmid (h) and RSP3 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the RSPH3 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by RSP3 HDR Plasmid (h) and RSP3 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by RSPH3 homology arms to support homology-directed repair at defined RSPH3 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.