FTS CRISPR/Cas9 KO Plasmid (m): sc-420422
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FTS 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 FTS 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: FTS Antibody (KK-L5): sc-134343
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FTS CRISPR/Cas9 KO Plasmid (m) | sc-420422 | 20 µg | $397.00 |
Overview
Mouse Aktip encodes the FTS protein, a component of the telomere regulatory machinery that associates with shelterin factors and helps maintain telomere integrity. FTS has been linked to control of telomerase access, telomere length homeostasis, and protection of chromosome ends, thereby influencing genome stability and proliferative capacity. Through these roles, Aktip/FTS intersects with DNA damage response and cell-cycle checkpoint signaling, processes frequently perturbed in chromosomal instability phenotypes and cancer-relevant models. Dissecting FTS function is also informative for studies of stem cell self-renewal, replicative stress, and aging-associated telomere dysfunction in mouse systems.
FTS CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Aktip gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Aktip 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 Aktip 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 FTS protein expression.
This CRISPR knockout system enables efficient generation of Aktip-deficient cell models for investigation of FTS signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Aktip exon(s) critical for FTS 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 Aktip genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by FTS CRISPR/Cas9 KO Plasmid (m) and FTS CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Aktip locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by FTS HDR Plasmid (m) and FTS HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Aktip homology arms to support homology-directed repair at defined Aktip 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.