
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CETP CRISPR Activation Plasmid (h) | sc-405829-ACT | 20 µg | $397.00 |
Human CETP (cholesteryl ester transfer protein) is a secreted plasma glycoprotein that mediates the transfer of cholesteryl esters and triglycerides between HDL and apoB-containing lipoproteins, shaping lipoprotein remodeling and reverse cholesterol transport. By regulating HDL-C distribution and lipid flux, CETP influences pathways governing lipid homeostasis, lipoprotein particle composition, and hepatobiliary clearance of cholesterol. Altered CETP activity or expression has been associated with dyslipidemia phenotypes and variation in cardiovascular and metabolic disease risk, making it a widely studied node in lipid metabolism research.
CETP CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CETP expression without altering the underlying DNA sequence.
CETP CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CETP 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 CETP transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CETP expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CETP locus and enabling the study of CETP-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CETP pathway restoration in tumor cells with silenced or reduced CETP expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.