
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Syntaxin 11 CRISPR Activation Plasmid (h) | sc-404809-ACT | 20 µg | $397.00 |
STX11 encodes syntaxin 11, a t-SNARE protein that regulates vesicle docking and membrane fusion events critical for regulated exocytosis and endosomal trafficking. In immune cells, Syntaxin 11 supports cytotoxic granule release and contributes to coordinated secretory lysosome dynamics that shape antiviral and antitumor responses. Disruption of STX11-dependent membrane fusion perturbs granule maturation and degranulation pathways, with documented relevance to primary immunodeficiency phenotypes involving defective lymphocyte cytotoxicity. As a component of SNARE-mediated trafficking networks, Syntaxin 11 is also used to study organelle identity, vesicle tethering, and cargo delivery in hematopoietic and inflammatory contexts.
Syntaxin 11 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous STX11 expression without altering the underlying DNA sequence.
Syntaxin 11 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the STX11 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 STX11 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Syntaxin 11 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native STX11 locus and enabling the study of Syntaxin 11-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Syntaxin 11 pathway restoration in tumor cells with silenced or reduced STX11 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.