FRAT1 CRISPR/Cas9 KO Plasmid (h): sc-406922
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FRAT1 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 FRAT1 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 | |
FRAT1 CRISPR/Cas9 KO Plasmid (h) | sc-406922 | 20 µg | $397.00 |
Overview
FRAT1 (frequently rearranged in advanced T-cell lymphomas 1) encodes a positive regulator of the Wnt/β-catenin pathway that promotes signaling output through inhibition of GSK3-dependent phosphorylation events, thereby stabilizing β-catenin and enhancing transcriptional programs linked to proliferation and differentiation. By modulating cytoplasmic and nuclear components of Wnt signaling, FRAT1 influences cell fate decisions, cell-cycle progression, and context-dependent control of migration. Altered FRAT1 expression has been reported in multiple tumor types and is frequently studied as a node connecting Wnt pathway activity to oncogenic transcriptional networks. FRAT1 is therefore relevant for dissecting pathway crosstalk affecting stem-like states, epithelial–mesenchymal transition-associated programs, and signal-dependent transcriptional regulation in human cells.
FRAT1 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the FRAT1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the FRAT1 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 FRAT1 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 FRAT1 protein expression.
This CRISPR knockout system enables efficient generation of FRAT1-deficient cell models for investigation of FRAT1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting FRAT1 exon(s) critical for FRAT1 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 FRAT1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by FRAT1 CRISPR/Cas9 KO Plasmid (h) and FRAT1 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the FRAT1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by FRAT1 HDR Plasmid (h) and FRAT1 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by FRAT1 homology arms to support homology-directed repair at defined FRAT1 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.