ACBP CRISPR/Cas9 KO Plasmid (m): sc-419950
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ACBP 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 ACBP 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 | |
ACBP CRISPR/Cas9 KO Plasmid (m) | sc-419950 | 20 µg | $397.00 |
Overview
Dbi encodes acyl-CoA–binding protein (ACBP), a conserved lipid chaperone that binds medium- and long-chain acyl-CoA esters and regulates their intracellular availability. In mouse cells, ACBP supports fatty acid trafficking and metabolic homeostasis by influencing β-oxidation, lipid synthesis, and membrane lipid remodeling, and it can modulate signaling networks linked to energy balance and cellular stress responses. Through these roles, DBI/ACBP is commonly studied in pathways connecting lipid metabolism to mitochondrial function, autophagy, and inflammation. Dysregulated acyl-CoA handling and lipid flux are relevant to models of metabolic dysfunction, neurobiology, and tumor cell lipid dependency, making Dbi a useful target for mechanistic studies.
ACBP CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Dbi gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Dbi 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 Dbi 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 ACBP protein expression.
This CRISPR knockout system enables efficient generation of Dbi-deficient cell models for investigation of ACBP signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Dbi exon(s) critical for ACBP 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 Dbi genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ACBP CRISPR/Cas9 KO Plasmid (m) and ACBP CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Dbi locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ACBP HDR Plasmid (m) and ACBP HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Dbi homology arms to support homology-directed repair at defined Dbi 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.