survivin CRISPR Activation Plasmid (h): sc-400205-ACT

BIRC5 encodes survivin, a multifunctional inhibitor of apoptosis protein that also serves as a core component of the chromosomal passenger complex to coordinate mitotic progression, chromosome segregation, and cytokinesis. Survivin integrates signaling inputs that govern cell-cycle checkpoint control and cell survival by modulating caspase activity and mitotic spindle dynamics. Dysregulated BIRC5 expression is frequently associated with elevated proliferation and apoptosis resistance, making it widely used as a molecular marker in studies of oncogenic signaling, genome stability, and stress-response pathways. As a human gene with strong cell-cycle dependence, BIRC5 provides a tractable node for interrogating mitosis-linked transcriptional programs and proteostasis networks in diverse cellular models.

survivin CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous BIRC5 expression without altering the underlying DNA sequence.

survivin CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the BIRC5 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 BIRC5 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous survivin expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native BIRC5 locus and enabling the study of survivin-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of survivin pathway restoration in tumor cells with silenced or reduced BIRC5 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.