Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
ACSL5 CRISPR/Cas9 KO Plasmid (m): sc-436628
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ACSL5 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 ACSL5 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: ACSL5 Antibody (A-2): sc-365478
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ACSL5 CRISPR/Cas9 KO Plasmid (m) | sc-436628 | 20 µg | $397.00 |
Overview
Acsl5 encodes acyl-CoA synthetase long-chain family member 5 (ACSL5), a mitochondrial/ER-associated enzyme that activates long-chain fatty acids to acyl-CoA thioesters, committing them to β-oxidation, triglyceride synthesis, and phospholipid remodeling. By shaping acyl-CoA pool composition, ACSL5 influences energy homeostasis, membrane lipid composition, and lipid-derived signaling pathways linked to mitochondrial metabolism and oxidative stress. In mouse tissues with high metabolic demand, altered ACSL5 activity has been associated with perturbations in fatty acid utilization and insulin-sensitive pathways, supporting its relevance to studies of metabolic dysregulation and lipid-associated inflammatory phenotypes.
ACSL5 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Acsl5 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Acsl5 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 Acsl5 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 ACSL5 protein expression.
This CRISPR knockout system enables efficient generation of Acsl5-deficient cell models for investigation of ACSL5 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Acsl5 exon(s) critical for ACSL5 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 Acsl5 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ACSL5 CRISPR/Cas9 KO Plasmid (m) and ACSL5 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Acsl5 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ACSL5 HDR Plasmid (m) and ACSL5 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Acsl5 homology arms to support homology-directed repair at defined Acsl5 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.