
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Septin 7 CRISPR Activation Plasmid (h) | sc-401655-ACT | 20 µg | $397.00 |
Human SEPT7 encodes septin 7, a core component of hetero-oligomeric septin filaments that function as diffusion barriers and cytoskeletal scaffolds. Septin 7 coordinates actin and microtubule organization to support cytokinesis, cell polarity, membrane remodeling, and vesicle trafficking, and it contributes to midbody architecture during cell division. Through these roles, SEPT7 influences processes linked to proliferation and migration and is frequently studied in the context of cytoskeletal dysregulation observed in cancer biology and neuroinflammatory or neurodegenerative disease mechanisms. Its interactions within septin complexes also connect SEPT7 to pathways governing cortical stability, cell shape control, and compartmentalization of membrane proteins.
Septin 7 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SEPT7 expression without altering the underlying DNA sequence.
Septin 7 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SEPT7 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 SEPT7 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Septin 7 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SEPT7 locus and enabling the study of Septin 7-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Septin 7 pathway restoration in tumor cells with silenced or reduced SEPT7 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.