ATP5S CRISPR/Cas9 KO Plasmid (h): sc-406318
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ATP5S CRISPR/Cas9 Knockout (KO) Plasmid (h) 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 ATP5S 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 | |
ATP5S CRISPR/Cas9 KO Plasmid (h) | sc-406318 | 20 µg | $397.00 |
Overview
ATP5S encodes a small accessory component of the mitochondrial F1F0 ATP synthase complex (Complex V), which catalyzes ATP production using the proton motive force generated by oxidative phosphorylation. Proper ATP5S function supports mitochondrial bioenergetics, maintenance of membrane potential, and coordination of cellular energy metabolism with processes such as apoptosis and reactive oxygen species homeostasis. Perturbations in ATP synthase assembly or Complex V activity are linked to mitochondrial dysfunction, a hallmark observed across a range of conditions including neuromuscular and neurodegenerative phenotypes as well as tumor metabolic remodeling. As a result, ATP5S is relevant for studies of mitochondrial respiration, energy stress responses, and mitochondrial signaling pathways that influence cell fate decisions.
ATP5S CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the ATP5S gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the ATP5S 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 ATP5S 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 ATP5S protein expression.
This CRISPR knockout system enables efficient generation of ATP5S-deficient cell models for investigation of ATP5S signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting ATP5S exon(s) critical for ATP5S 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 ATP5S genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ATP5S CRISPR/Cas9 KO Plasmid (h) and ATP5S CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the ATP5S locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ATP5S HDR Plasmid (h) and ATP5S HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by ATP5S homology arms to support homology-directed repair at defined ATP5S 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.