follistatin CRISPR/Cas9 KO Plasmid (m): sc-420417
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- follistatin 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 follistatin 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: follistatin Antibody (C-8): sc-365003
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
follistatin CRISPR/Cas9 KO Plasmid (m) | sc-420417 | 20 µg | $397.00 |
Overview
Mouse Fst encodes follistatin, a secreted glycoprotein that binds and neutralizes TGF-β superfamily ligands, particularly activins and several BMPs, thereby modulating SMAD2/3- and SMAD1/5/8-dependent transcriptional programs. By limiting ligand availability, follistatin shapes cell fate decisions, tissue growth, and repair processes across muscle, reproductive, and metabolic systems. Fst activity influences myogenesis and fibrosis-related remodeling, and dysregulated activin–follistatin balance is studied in contexts of muscle wasting, inflammatory signaling, and reproductive phenotypes. As a key extracellular regulator of growth factor signaling, Fst provides a tractable node for dissecting pathway crosstalk and feedback in developmental and homeostatic circuits.
follistatin CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Fst gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Fst 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 Fst 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 follistatin protein expression.
This CRISPR knockout system enables efficient generation of Fst-deficient cell models for investigation of follistatin signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Fst exon(s) critical for follistatin 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 Fst genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by follistatin CRISPR/Cas9 KO Plasmid (m) and follistatin CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Fst locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by follistatin HDR Plasmid (m) and follistatin HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Fst homology arms to support homology-directed repair at defined Fst 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.