
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SSX5 CRISPR Activation Plasmid (h) | sc-403552-ACT | 20 µg | $397.00 |
SSX5 (synovial sarcoma, X breakpoint 5) encodes a cancer-testis antigen–like nuclear protein implicated in transcriptional regulation and chromatin-associated processes. SSX family members can interact with epigenetic regulators, including Polycomb group complexes, influencing gene expression programs linked to cell identity and proliferative control. Aberrant SSX5 expression has been reported in multiple tumor contexts and is frequently studied in the setting of SSX-associated fusion oncogenes and immune-oncology antigen biology. As a result, SSX5 is used as a model to investigate transcriptional dysregulation, lineage-restricted antigen expression, and tumor-associated regulatory networks.
SSX5 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SSX5 expression without altering the underlying DNA sequence.
SSX5 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SSX5 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 SSX5 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SSX5 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SSX5 locus and enabling the study of SSX5-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SSX5 pathway restoration in tumor cells with silenced or reduced SSX5 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.