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.
β-TrCP CRISPR/Cas9 KO Plasmid (h): sc-400971
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- β-TrCP 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 β-TrCP 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: β-TrCP Antibody (C-6): sc-390629
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
β-TrCP CRISPR/Cas9 KO Plasmid (h) | sc-400971 | 20 µg | $397.00 |
Overview
BTRC encodes the F-box protein β-TrCP, a substrate recognition component of the SCF (SKP1–CUL1–F-box) E3 ubiquitin ligase complex that targets phosphorylated degron motifs for ubiquitination and proteasomal turnover. β-TrCP regulates multiple signaling axes, including NF-κB signaling via IκB turnover, Wnt/β-catenin signaling through β-catenin degradation, and cell-cycle control by modulating proteins such as CDC25A and EMI1. Through these pathways, BTRC influences proliferation, inflammatory responses, DNA damage adaptation, and epithelial–mesenchymal programs. Dysregulated β-TrCP activity has been associated with aberrant pathway activation and genomic instability in diverse cancer and immune-related research contexts.
β-TrCP CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the BTRC gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the BTRC 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 BTRC 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 β-TrCP protein expression.
This CRISPR knockout system enables efficient generation of BTRC-deficient cell models for investigation of β-TrCP signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting BTRC exon(s) critical for β-TrCP 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 BTRC genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by β-TrCP CRISPR/Cas9 KO Plasmid (h) and β-TrCP CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the BTRC locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by β-TrCP HDR Plasmid (h) and β-TrCP HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by BTRC homology arms to support homology-directed repair at defined BTRC 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.