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.
FAS CRISPR/Cas9 KO Plasmid (m): sc-420287
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FAS 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 FAS 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: FAS Antibody (C236): sc-21730
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FAS CRISPR/Cas9 KO Plasmid (m) | sc-420287 | 20 µg | $397.00 |
Overview
Fas encodes FAS (CD95/APO-1), a death receptor of the TNF receptor superfamily that initiates extrinsic apoptosis upon engagement by FAS ligand and subsequent formation of the death-inducing signaling complex (DISC). This signaling cascade recruits FADD and activates CASP8/CASP10, linking to downstream effector caspases and intersecting with mitochondrial apoptosis and NF-κB–associated survival programs depending on cellular context. In mouse immune homeostasis, FAS-mediated activation-induced cell death constrains lymphocyte expansion and supports peripheral tolerance. Dysregulated Fas/FAS signaling is associated with defective apoptosis, chronic immune activation, lymphoproliferation, and altered tissue injury responses in inflammation models.
FAS CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Fas gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Fas 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 Fas 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 FAS protein expression.
This CRISPR knockout system enables efficient generation of Fas-deficient cell models for investigation of FAS signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Fas exon(s) critical for FAS 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 Fas genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by FAS CRISPR/Cas9 KO Plasmid (m) and FAS CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Fas locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by FAS HDR Plasmid (m) and FAS HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Fas homology arms to support homology-directed repair at defined Fas 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.