
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
survivin Lentiviral Activation Particles (h) | sc-400205-LAC | 200 µl | $455.00 |
Human BIRC5 encodes survivin, a bifunctional inhibitor of apoptosis (IAP) family protein that coordinates mitotic progression and cell survival. Survivin is a core component of the chromosomal passenger complex, supporting kinetochore–microtubule attachment, spindle checkpoint control, and cytokinesis, while also modulating caspase-dependent apoptotic signaling. BIRC5 expression is tightly linked to cell-cycle regulation and stress responses, with elevated levels frequently associated with proliferative states and dysregulated apoptosis in cancer biology. As a nodal regulator connecting mitosis and survival pathways, survivin is widely studied in mechanisms of genomic instability, therapy response phenotypes, and biomarker-driven pathway analyses.
survivin 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 BIRC5 upregulation across a broader range of human cell types.
survivin 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 BIRC5 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous survivin expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native BIRC5 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.