
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SSX5 Lentiviral Activation Particles (h) | sc-403552-LAC | 200 µl | $455.00 |
SSX5 (synovial sarcoma, X breakpoint 5) encodes a nuclear cancer-testis antigen and transcriptional regulator that can modulate chromatin-associated gene expression programs in a context-dependent manner. SSX5 has been implicated in transcriptional repression complexes and altered epigenetic states that influence cell identity, differentiation, and proliferative capacity. Aberrant expression of SSX family members is associated with tumor biology and immune-restricted expression patterns, making SSX5 a useful model for studying lineage-restricted transcriptional networks. In human cells, SSX5 is commonly investigated for its contributions to dysregulated gene regulation, protein–protein interactions, and cancer-associated transcriptional circuitry.
SSX5 Lentiviral Activation Particles (h) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient SSX5 upregulation across a broader range of human cell types.
SSX5 Lentiviral Activation Particles (h) deliver all functional components of the synergistic activation mediator (SAM) system via lentiviral transduction. The system comprises three particle preparations co-transduced into target cells: one encoding catalytically inactive dCas9 (D10A and N863A mutations) fused to the VP64 transactivation domain with a blasticidin resistance gene; one encoding the MS2-p65-HSF1 fusion protein with a hygromycin resistance gene; and one encoding a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers with a puromycin resistance gene. Following lentiviral transduction and genomic integration of the expression cassettes, the SAM components are stably expressed and assemble at the target locus within the proximal promoter region upstream of the SSX5 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous SSX5 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native SSX5 genomic locus and regulatory architecture.
The lentiviral format offers several practical advantages: stable genomic integration supports heritable activation across cell divisions; high-titer particle preparations eliminate the need for in-house viral production; and compatibility with primary, non-dividing, and transfection-resistant cell types expands experimental accessibility. Successful transduction can be confirmed and enriched through triple antibiotic selection using puromycin, hygromycin, and blasticidin.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.