
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SSX7 CRISPR Activation Plasmid (h) | sc-403553-ACT | 20 µg | $397.00 |
SSX7 (synovial sarcoma, X breakpoint 7) encodes a cancer-testis antigen–like protein within the SSX family, characterized by restricted normal expression and roles in transcriptional regulation. SSX7 is thought to participate in chromatin-associated processes and modulation of gene expression programs that influence cell identity and proliferation. Dysregulated SSX family expression has been linked to tumor-associated transcriptional states and immunogenic antigen presentation, supporting its utility as a molecular marker in cancer biology. Studying SSX7 helps clarify mechanisms of epigenetic control, transcriptional repression/activation balance, and downstream pathway remodeling in transformed cells.
SSX7 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SSX7 expression without altering the underlying DNA sequence.
SSX7 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SSX7 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 SSX7 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SSX7 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SSX7 locus and enabling the study of SSX7-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SSX7 pathway restoration in tumor cells with silenced or reduced SSX7 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.