SET7/9 CRISPR Activation Plasmid (h): sc-405251-ACT

Human SETD7 (SET7/9) is a SET domain-containing lysine methyltransferase that primarily monomethylates histone H3 at Lys4 (H3K4me1) and can also modify non-histone substrates, linking chromatin state to transcriptional control. Through these epigenetic and protein-methylation activities, SET7/9 influences cell-cycle progression, differentiation programs, stress responses, and metabolic gene regulation. SETD7-dependent signaling intersects with pathways governed by major transcription factors and regulatory hubs, shaping context-specific gene expression outputs. Dysregulated SETD7 activity or expression has been associated with altered transcriptional networks observed across cancer biology, inflammation, and cardiometabolic disease models, making it a useful node for mechanistic studies of epigenetic regulation.

SET7/9 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SETD7 expression without altering the underlying DNA sequence.

SET7/9 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SETD7 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 SETD7 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SET7/9 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SETD7 locus and enabling the study of SET7/9-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SET7/9 pathway restoration in tumor cells with silenced or reduced SETD7 expression.

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