KIF3A CRISPR/Cas9 KO Plasmid (m): sc-421275
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- KIF3A 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 KIF3A 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: KIF3A Antibody (E-5): sc-376680
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
KIF3A CRISPR/Cas9 KO Plasmid (m) | sc-421275 | 20 µg | $397.00 |
Overview
Kif3a encodes the kinesin family member KIF3A, a core motor subunit of the heterotrimeric kinesin-2 complex that drives anterograde intraflagellar transport along microtubules. KIF3A is essential for primary cilium assembly and maintenance, enabling cilia-dependent signal transduction including Hedgehog pathway activity and broader ciliary trafficking processes that influence cell fate decisions. In mouse systems, Kif3a function is closely tied to tissue morphogenesis and homeostatic signaling programs that rely on intact cilia, linking its perturbation to ciliopathy-relevant phenotypes. As a result, KIF3A is frequently used to dissect how microtubule-based transport interfaces with developmental signaling and cilium-mediated regulation of proliferation and differentiation.
KIF3A CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Kif3a gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Kif3a 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 Kif3a 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 KIF3A protein expression.
This CRISPR knockout system enables efficient generation of Kif3a-deficient cell models for investigation of KIF3A signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Kif3a exon(s) critical for KIF3A 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 Kif3a genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by KIF3A CRISPR/Cas9 KO Plasmid (m) and KIF3A CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Kif3a locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by KIF3A HDR Plasmid (m) and KIF3A HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Kif3a homology arms to support homology-directed repair at defined Kif3a 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.