Endothelial Lipase CRISPR/Cas9 KO Plasmid (h): sc-406307
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Endothelial Lipase CRISPR/Cas9 Knockout (KO) Plasmid (h) 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 Endothelial Lipase 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: Endothelial Lipase Antibody (4A9): sc-517036
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Endothelial Lipase CRISPR/Cas9 KO Plasmid (h) | sc-406307 | 20 µg | $397.00 |
Overview
LIPG encodes endothelial lipase (EL), a secreted phospholipase A1 expressed by vascular endothelium that hydrolyzes phospholipids in circulating HDL and modulates lipoprotein remodeling and cholesterol transport. By regulating HDL catabolism and phospholipid turnover, EL influences vascular lipid homeostasis and intersects with inflammatory signaling in endothelial cells and macrophages. Altered LIPG activity and expression have been associated with dyslipidemia-related phenotypes and atherosclerosis-relevant processes, including endothelial dysfunction and lipid-driven vascular inflammation. LIPG is also studied for its impact on extracellular lipase networks with LPL and hepatic lipase, and for effects on lipid mediator production.
Endothelial Lipase CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the LIPG gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the LIPG 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 LIPG 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 Endothelial Lipase protein expression.
This CRISPR knockout system enables efficient generation of LIPG-deficient cell models for investigation of Endothelial Lipase signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting LIPG exon(s) critical for Endothelial Lipase 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 LIPG genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Endothelial Lipase CRISPR/Cas9 KO Plasmid (h) and Endothelial Lipase CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the LIPG locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Endothelial Lipase HDR Plasmid (h) and Endothelial Lipase HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by LIPG homology arms to support homology-directed repair at defined LIPG 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.