Fnk CRISPR/Cas9 KO Plasmid (m): sc-419717
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Fnk 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 Fnk 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 | |
Fnk CRISPR/Cas9 KO Plasmid (m) | sc-419717 | 20 µg | $397.00 |
Overview
Mouse Plk3 encodes the serine/threonine kinase Fnk, a Polo-like kinase family member implicated in stress-responsive signaling and cell-cycle control. Fnk participates in checkpoint regulation and modulates pathways linked to DNA damage responses, apoptosis, and proliferation through phosphorylation-dependent signaling networks. Altered PLK3/Fnk activity has been associated with dysregulated mitotic progression and genome stability phenotypes that are relevant to cancer biology and tissue homeostasis. These properties make Plk3 a useful target for probing kinase-regulated signaling, stress adaptation, and cell fate decisions in mammalian model systems.
Fnk CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Plk3 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Plk3 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 Plk3 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 Fnk protein expression.
This CRISPR knockout system enables efficient generation of Plk3-deficient cell models for investigation of Fnk signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Plk3 exon(s) critical for Fnk 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 Plk3 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Fnk CRISPR/Cas9 KO Plasmid (m) and Fnk CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Plk3 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Fnk HDR Plasmid (m) and Fnk HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Plk3 homology arms to support homology-directed repair at defined Plk3 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.