PRIC285 CRISPR Activation Plasmid (h): sc-406441-ACT

Human HELZ2 (also referred to as PRIC285) encodes a helicase-like transcriptional coactivator that integrates signals from nuclear hormone receptors and other transcription factors to modulate RNA polymerase II–dependent gene expression. PRIC285 has been linked to regulation of lipid and glucose metabolism programs through interactions with pathways such as PPAR signaling, influencing cellular energy homeostasis and inflammatory tone. By shaping transcriptional outputs in hepatocytes, adipocytes, and immune-relevant contexts, HELZ2 activity is studied for its contributions to metabolic dysregulation and related complex disease phenotypes. Its nuclear coactivator function also makes it useful for dissecting chromatin-dependent control of inducible gene networks and stress-responsive transcription.

PRIC285 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous HELZ2 expression without altering the underlying DNA sequence.

PRIC285 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the HELZ2 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 HELZ2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous PRIC285 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native HELZ2 locus and enabling the study of PRIC285-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of PRIC285 pathway restoration in tumor cells with silenced or reduced HELZ2 expression.

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