CEL CRISPR Activation Plasmid (h): sc-403176-ACT

Human CEL encodes carboxyl ester lipase, a secreted lipolytic enzyme best known for hydrolyzing cholesteryl esters and triglycerides in the intestinal lumen and contributing to dietary lipid absorption. CEL activity intersects with lipid trafficking and lipoprotein remodeling processes that influence cellular cholesterol homeostasis and metabolic signaling. Expression has also been described in pancreatic acinar tissue and milk, linking CEL to digestive physiology and nutrient handling across developmental contexts. Genetic variation or dysregulated expression of CEL has been associated with altered lipid metabolism phenotypes and pancreatic dysfunction, providing a mechanistic entry point for studies of metabolic and exocrine pathways.

CEL CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CEL expression without altering the underlying DNA sequence.

CEL CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CEL locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.

Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the CEL transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CEL expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CEL locus and enabling the study of CEL-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CEL pathway restoration in tumor cells with silenced or reduced CEL expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.