PRMT6 CRISPR Activation Plasmid (h): sc-403433-ACT

PRMT6 (protein arginine methyltransferase 6) is a nuclear type I PRMT that catalyzes asymmetric dimethylation of arginine residues on histones and non-histone substrates, thereby modulating chromatin structure and transcriptional programs. It contributes to epigenetic regulation through histone H3 arginine methylation and cross-talk with other post-translational modifications, influencing cell cycle progression, DNA damage responses, and differentiation-associated gene expression. PRMT6 activity interfaces with pathways governing transcriptional repression/activation and chromatin remodeling complexes, shaping context-specific gene regulatory networks. Dysregulated PRMT6 expression or activity has been reported in multiple disease-relevant settings, supporting its utility as a target for mechanistic studies of epigenetic control and gene expression plasticity in human cells.

PRMT6 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous PRMT6 expression without altering the underlying DNA sequence.

PRMT6 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the PRMT6 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 PRMT6 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous PRMT6 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native PRMT6 locus and enabling the study of PRMT6-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of PRMT6 pathway restoration in tumor cells with silenced or reduced PRMT6 expression.

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