ATGL CRISPR/Cas9 KO Plasmid (m): sc-426224
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ATGL 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 ATGL 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: ATGL Antibody (F-7): sc-365278
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ATGL CRISPR/Cas9 KO Plasmid (m) | sc-426224 | 20 µg | $397.00 |
Overview
Mouse Pnpla2 encodes adipose triglyceride lipase (ATGL), a key rate-limiting enzyme that initiates cytosolic triglyceride hydrolysis to generate diacylglycerol and free fatty acids for mitochondrial β-oxidation and lipid signaling. ATGL activity coordinates lipolysis with energy homeostasis and interfaces with lipid droplet turnover, PPAR-mediated transcriptional programs, and insulin-responsive metabolic pathways. Perturbation of ATGL-dependent lipolysis alters cellular lipid storage and fatty acid flux, linking Pnpla2 to dysregulated lipid metabolism and stress responses in metabolically active tissues. These features make ATGL a widely used target for mechanistic studies of lipid droplet biology, nutrient sensing, and metabolic remodeling.
ATGL CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Pnpla2 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Pnpla2 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 Pnpla2 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 ATGL protein expression.
This CRISPR knockout system enables efficient generation of Pnpla2-deficient cell models for investigation of ATGL signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Pnpla2 exon(s) critical for ATGL 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 Pnpla2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ATGL CRISPR/Cas9 KO Plasmid (m) and ATGL CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Pnpla2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ATGL HDR Plasmid (m) and ATGL HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Pnpla2 homology arms to support homology-directed repair at defined Pnpla2 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.