TSGA2 CRISPR/Cas9 KO Plasmid (m): sc-423525
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TSGA2 CRISPR/Cas9 Knockout (KO) Plasmid (m) 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 TSGA2 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 | |
TSGA2 CRISPR/Cas9 KO Plasmid (m) | sc-423525 | 20 µg | $397.00 |
Overview
Rsph1 encodes a radial spoke head component required for proper axonemal architecture and coordinated ciliary and flagellar beating, supporting motile ciliogenesis and microtubule-based transport in multiciliated epithelia. Through its role in the 9+2 axoneme, RSPH1 contributes to pathways that govern mucociliary clearance and sperm motility, linking its function to airway homeostasis and reproductive biology. Disruption of radial spoke proteins is associated with primary ciliary dyskinesia phenotypes, including chronic respiratory disease and laterality defects, making Rsph1 a useful locus for studying cilia-driven developmental and inflammatory processes. In mouse models, Rsph1 perturbation enables mechanistic interrogation of motile cilia structure–function relationships across respiratory and reproductive tissues.
TSGA2 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Rsph1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Rsph1 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 Rsph1 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 TSGA2 protein expression.
This CRISPR knockout system enables efficient generation of Rsph1-deficient cell models for investigation of TSGA2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Rsph1 exon(s) critical for TSGA2 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 Rsph1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TSGA2 CRISPR/Cas9 KO Plasmid (m) and TSGA2 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Rsph1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TSGA2 HDR Plasmid (m) and TSGA2 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Rsph1 homology arms to support homology-directed repair at defined Rsph1 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.