Slfn3 CRISPR/Cas9 KO Plasmid (m): sc-423018
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Slfn3 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 Slfn3 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 | |
Slfn3 CRISPR/Cas9 KO Plasmid (m) | sc-423018 | 20 µg | $397.00 |
Overview
Slfn3 (schlafen 3) encodes a member of the Schlafen family implicated in regulation of cellular differentiation, proliferation, and immune-associated programs in mouse tissues. Schlafen proteins are commonly linked to interferon-responsive signaling, modulation of translation and RNA metabolism, and context-dependent control of cell-cycle progression. In epithelial models, Slfn3 has been studied as a factor associated with differentiation state and barrier-related gene expression, connecting it to pathways that influence tissue homeostasis and inflammatory responses. Altered schlafen-family activity has been investigated in settings of immune dysregulation and tumor biology, making Slfn3 a useful target for mechanistic studies of growth control and immune signaling networks.
Slfn3 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Slfn3 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Slfn3 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 Slfn3 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 Slfn3 protein expression.
This CRISPR knockout system enables efficient generation of Slfn3-deficient cell models for investigation of Slfn3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Slfn3 exon(s) critical for Slfn3 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 Slfn3 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Slfn3 CRISPR/Cas9 KO Plasmid (m) and Slfn3 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Slfn3 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Slfn3 HDR Plasmid (m) and Slfn3 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Slfn3 homology arms to support homology-directed repair at defined Slfn3 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.