
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
apoC1 CRISPR Activation Plasmid (h) | sc-403713-ACT | 20 µg | $397.00 |
Human APOC1 encodes apolipoprotein C-I (apoC1), a small, exchangeable apolipoprotein that associates with HDL and triglyceride-rich lipoproteins to modulate lipid transport and clearance. apoC1 influences lipoprotein remodeling by regulating interactions with lipases and receptors, including effects on VLDL metabolism and cholesterol homeostasis. Through these functions, APOC1 contributes to pathways linking hepatic lipid handling, macrophage foam cell biology, and inflammatory signaling within the vascular microenvironment. Altered APOC1 expression has been reported in dyslipidemia and cardiometabolic phenotypes, and is also studied in neuroinflammation and Alzheimer’s disease-related lipid pathways.
apoC1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous APOC1 expression without altering the underlying DNA sequence.
apoC1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the APOC1 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 APOC1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous apoC1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native APOC1 locus and enabling the study of apoC1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of apoC1 pathway restoration in tumor cells with silenced or reduced APOC1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.