ATP11C CRISPR/Cas9 KO Plasmid (m): sc-435843
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ATP11C 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 ATP11C 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 | |
ATP11C CRISPR/Cas9 KO Plasmid (m) | sc-435843 | 20 µg | $397.00 |
Overview
Atp11c encodes ATP11C, a P4-ATPase phospholipid flippase that maintains plasma membrane lipid asymmetry by translocating aminophospholipids such as phosphatidylserine from the outer to inner leaflet. This activity supports vesicle trafficking, endocytosis, and membrane remodeling processes that influence receptor signaling and cell survival programs. In mouse, ATP11C function has been linked to hematopoietic and immune system homeostasis, with perturbation affecting B cell development and erythroid biology, making it relevant to studies of immunodeficiency-like phenotypes and anemia-related mechanisms. Altered membrane lipid distribution controlled by ATP11C can also modulate apoptotic cell clearance and inflammatory signaling through exposure of phosphatidylserine at the cell surface.
ATP11C CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Atp11c gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Atp11c 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 Atp11c 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 ATP11C protein expression.
This CRISPR knockout system enables efficient generation of Atp11c-deficient cell models for investigation of ATP11C signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Atp11c exon(s) critical for ATP11C 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 Atp11c genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ATP11C CRISPR/Cas9 KO Plasmid (m) and ATP11C CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Atp11c locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ATP11C HDR Plasmid (m) and ATP11C HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Atp11c homology arms to support homology-directed repair at defined Atp11c 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.