
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HES6 CRISPR Activation Plasmid (h) | sc-404146-ACT | 20 µg | $397.00 |
HES6 (hairy and enhancer of split 6) encodes a basic helix-loop-helix transcriptional regulator that modulates Notch pathway outputs and influences lineage commitment during development. In human cells, HES6 can antagonize HES1-mediated repression and interface with neurogenic and myogenic transcriptional programs to shape differentiation and proliferative states. Dysregulated HES6 expression has been reported in multiple tumor contexts and is used as a mechanistic handle for studying transcriptional rewiring, cellular plasticity, and context-dependent control of cell fate. These features make HES6 a useful node for investigating gene regulatory networks downstream of Notch and bHLH signaling.
HES6 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous HES6 expression without altering the underlying DNA sequence.
HES6 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the HES6 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 HES6 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous HES6 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native HES6 locus and enabling the study of HES6-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of HES6 pathway restoration in tumor cells with silenced or reduced HES6 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.