
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
AdipoR2 CRISPR Activation Plasmid (h) | sc-401848-ACT | 20 µg | $397.00 |
ADIPOR2 encodes adiponectin receptor 2 (AdipoR2), a seven-transmembrane receptor that mediates adiponectin-dependent metabolic signaling in multiple tissues. AdipoR2 activation supports fatty acid oxidation and glucose homeostasis, in part through AMPK- and PPARα-associated transcriptional programs, and influences cellular stress responses and inflammatory signaling. Altered ADIPOR2 expression or signaling has been linked to insulin resistance, metabolic syndrome, nonalcoholic fatty liver disease, and broader cardiometabolic risk, making it a relevant target for mechanistic studies of adipokine pathways.
AdipoR2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ADIPOR2 expression without altering the underlying DNA sequence.
AdipoR2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ADIPOR2 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 ADIPOR2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous AdipoR2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ADIPOR2 locus and enabling the study of AdipoR2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of AdipoR2 pathway restoration in tumor cells with silenced or reduced ADIPOR2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.