
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
EMSY CRISPR Activation Plasmid (h) | sc-405722-ACT | 20 µg | $397.00 |
EMSY encodes a nuclear chromatin-associated protein that binds BRCA2 and participates in the regulation of DNA damage responses, transcriptional control, and maintenance of genome stability. Through interactions with chromatin remodeling and repair factors, EMSY can influence homologous recombination competence, replication stress signaling, and cell-cycle checkpoint coordination. Altered EMSY expression or copy number has been linked to dysregulated DNA repair capacity and transcriptional programs that support oncogenic phenotypes in multiple tumor contexts. As a result, EMSY is frequently studied in pathways connecting chromatin dynamics, BRCA2-associated repair biology, and genome instability–driven disease mechanisms.
EMSY CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous EMSY expression without altering the underlying DNA sequence.
EMSY CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the EMSY 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 EMSY transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous EMSY expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native EMSY locus and enabling the study of EMSY-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of EMSY pathway restoration in tumor cells with silenced or reduced EMSY expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.