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.
Filensin CRISPR/Cas9 KO Plasmid (m): sc-419323
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Filensin 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 Filensin 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: Filensin Antibody (IB38): sc-69689
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Filensin CRISPR/Cas9 KO Plasmid (m) | sc-419323 | 20 µg | $397.00 |
Overview
Bfsp1 encodes filensin, a lens fiber cell–enriched intermediate filament protein that heteropolymerizes with phakinin (BFSP2) to form beaded filaments. This cytoskeletal network supports lens fiber cell architecture, contributes to organelle-free zone formation during terminal differentiation, and helps maintain refractive transparency through stabilization of membrane–cytoskeleton interactions. Disruption of beaded filament assembly perturbs lens biomechanics and proteostasis, linking BFSP1-associated filament defects to cataract-related phenotypes and broader pathways controlling cytoskeletal organization, protein aggregation, and cellular stress responses.
Filensin CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Bfsp1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Bfsp1 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 Bfsp1 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 Filensin protein expression.
This CRISPR knockout system enables efficient generation of Bfsp1-deficient cell models for investigation of Filensin signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Bfsp1 exon(s) critical for Filensin 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 Bfsp1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Filensin CRISPR/Cas9 KO Plasmid (m) and Filensin CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Bfsp1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Filensin HDR Plasmid (m) and Filensin HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Bfsp1 homology arms to support homology-directed repair at defined Bfsp1 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.