
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Daxx CRISPR Activation Plasmid (h) | sc-400686-ACT | 20 µg | $397.00 |
Human DAXX encodes the death domain–associated protein Daxx, a multifunctional nuclear factor implicated in transcriptional control, chromatin remodeling, and stress-responsive signaling. Daxx associates with ATRX and histone H3.3 to regulate heterochromatin organization, telomeric and pericentromeric integrity, and transposon repression, linking it to epigenetic maintenance pathways. It also localizes to PML nuclear bodies and modulates apoptotic and DNA damage response networks through interactions with diverse transcription factors and signaling mediators. Dysregulation of DAXX has been connected to altered genome stability and aberrant gene expression programs observed in multiple disease contexts, supporting its use as a mechanistic node in chromatin and stress pathway studies.
Daxx CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous DAXX expression without altering the underlying DNA sequence.
Daxx CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the DAXX 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 DAXX transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Daxx expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native DAXX locus and enabling the study of Daxx-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Daxx pathway restoration in tumor cells with silenced or reduced DAXX expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.