resistin CRISPR Activation Plasmid (h): sc-402649-ACT

Human RETN encodes resistin, a secreted cysteine-rich adipokine best known for linking metabolic status to inflammatory signaling. Resistin modulates insulin sensitivity and glucose homeostasis and can promote cytokine production through pathways such as NF-κB and MAPK signaling in immune and metabolic cell types. Altered RETN expression has been associated with obesity-related metabolic dysfunction, type 2 diabetes, and chronic low-grade inflammation, and it is also studied in cardiovascular and autoimmune disease contexts. As a circulating mediator, resistin is frequently used as a readout for adipose–immune crosstalk and stress-responsive transcriptional programs.

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

resistin CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the RETN 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 RETN transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous resistin expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native RETN locus and enabling the study of resistin-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of resistin pathway restoration in tumor cells with silenced or reduced RETN expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.