CD36 CRISPR Activation Plasmid (m): sc-419545-ACT

Mouse Cd36 encodes CD36, a multifunctional class B scavenger receptor that binds long-chain fatty acids and oxidized lipoproteins to regulate lipid uptake, intracellular lipid handling, and energy metabolism. CD36 participates in pathways controlling fatty acid transport, inflammatory signaling, and macrophage foam cell formation, linking nutrient sensing to innate immune responses. In addition to roles in adipose tissue, muscle, and liver metabolism, CD36 activity influences vascular biology and oxidative stress responses through interactions with modified lipids. Dysregulated Cd36 expression or signaling has been associated with cardiometabolic phenotypes, insulin resistance–related processes, and inflammation-driven pathologies in mouse models.

CD36 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Cd36 expression without altering the underlying DNA sequence.

CD36 CRISPR Activation Plasmid (m) 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.