FBL4 CRISPR/Cas9 KO Plasmid (m): sc-435345
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FBL4 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 FBL4 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: FBL4 Antibody (A-7): sc-376102
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FBL4 CRISPR/Cas9 KO Plasmid (m) | sc-435345 | 20 µg | $397.00 |
Overview
Fbxl4 encodes an F-box and leucine-rich repeat protein that functions as a substrate-recognition component of SCF (SKP1–CUL1–F-box) E3 ubiquitin ligase complexes, helping direct specific proteins toward ubiquitin-dependent turnover. Through regulated proteostasis, FBXL4 can influence cell cycle progression, stress responses, and broader ubiquitin–proteasome system dynamics. In mouse, altered FBXL4 activity has been linked to mitochondrial homeostasis and cellular energy metabolism, supporting its relevance for studies of mitochondrial dysfunction and associated multisystem disease phenotypes. Fbxl4 is therefore a useful target for dissecting how ubiquitin-mediated quality control interfaces with metabolic pathways and organelle maintenance.
FBL4 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Fbxl4 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Fbxl4 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 Fbxl4 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 FBL4 protein expression.
This CRISPR knockout system enables efficient generation of Fbxl4-deficient cell models for investigation of FBL4 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Fbxl4 exon(s) critical for FBL4 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 Fbxl4 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by FBL4 CRISPR/Cas9 KO Plasmid (m) and FBL4 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Fbxl4 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by FBL4 HDR Plasmid (m) and FBL4 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Fbxl4 homology arms to support homology-directed repair at defined Fbxl4 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.