
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CD36 CRISPR Activation Plasmid (h) | sc-400233-ACT | 20 µg | $397.00 |
Human CD36 encodes a multifunctional scavenger receptor that mediates uptake of long-chain fatty acids and oxidized lipoproteins, coordinating lipid handling with cellular metabolic state. CD36 participates in lipid transport and storage programs and interfaces with inflammatory signaling, including processes linked to macrophage activation and foam cell formation. Through its roles in endothelial, adipocyte, and immune cell biology, CD36 is frequently studied in pathways underlying atherosclerosis, metabolic dysfunction, and chronic inflammation. Altered CD36 activity has also been investigated in cancer cell metabolism and the tumor microenvironment, where lipid utilization can influence growth and immune phenotypes.
CD36 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CD36 expression without altering the underlying DNA sequence.
CD36 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CD36 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 CD36 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CD36 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CD36 locus and enabling the study of CD36-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CD36 pathway restoration in tumor cells with silenced or reduced CD36 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.