apoD CRISPR/Cas9 KO Plasmid (m): sc-419166
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- apoD 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 apoD 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: apoD Antibody (D-12): sc-166612
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
apoD CRISPR/Cas9 KO Plasmid (m) | sc-419166 | 20 µg | $397.00 |
Overview
Mouse Apod encodes apolipoprotein D (apoD), a lipocalin that binds hydrophobic ligands such as cholesterol, arachidonic acid, and lipid peroxidation products, supporting lipid transport and redox homeostasis. apoD expression is linked to responses to oxidative stress, inflammation, and cellular aging, and it can influence membrane lipid remodeling and lipoprotein-associated pathways in the nervous system and peripheral tissues. In brain and glia, apoD has been studied in contexts of myelination, synaptic maintenance, and injury responses, connecting Apod regulation to neurodegeneration-relevant processes. Altered apoD levels have also been associated with metabolic and inflammatory phenotypes, making Apod a useful node for dissecting lipid-handling mechanisms in disease-relevant models.
apoD CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Apod gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Apod 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 Apod 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 apoD protein expression.
This CRISPR knockout system enables efficient generation of Apod-deficient cell models for investigation of apoD signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Apod exon(s) critical for apoD 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 Apod genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by apoD CRISPR/Cas9 KO Plasmid (m) and apoD CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Apod locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by apoD HDR Plasmid (m) and apoD HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Apod homology arms to support homology-directed repair at defined Apod 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.