Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Rak CRISPR/Cas9 KO Plasmid (h): sc-405590
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Rak 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 Rak 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: Rak Antibody (H-12): sc-166478
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Rak CRISPR/Cas9 KO Plasmid (h) | sc-405590 | 20 µg | $397.00 |
Overview
Human FRK encodes Rak, a non-receptor tyrosine kinase of the BRK family that modulates signaling at the plasma membrane and in the nucleus. Rak has been linked to regulation of receptor tyrosine kinase pathways, cytoskeletal dynamics, and cell-cycle control through phosphorylation-dependent remodeling of downstream effectors. By influencing proliferation, differentiation, and cellular stress responses, FRK/Rak activity is studied in contexts of epithelial biology and oncogenic signaling networks. Altered FRK expression or kinase activity has been associated with changes in tumor cell behavior and signal transduction states, supporting its relevance as a mechanistic node in cancer-related pathways.
Rak CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the FRK gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the FRK 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 FRK 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 Rak protein expression.
This CRISPR knockout system enables efficient generation of FRK-deficient cell models for investigation of Rak signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting FRK exon(s) critical for Rak 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 FRK genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Rak CRISPR/Cas9 KO Plasmid (h) and Rak CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the FRK locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Rak HDR Plasmid (h) and Rak HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by FRK homology arms to support homology-directed repair at defined FRK 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.