
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Tomosyn CRISPR Activation Plasmid (h) | sc-403625-ACT | 20 µg | $397.00 |
Human STXBP5 encodes tomosyn, a syntaxin-binding protein that regulates SNARE complex assembly and vesicle priming to modulate membrane fusion and exocytosis. By interacting with plasma membrane t-SNAREs, tomosyn influences regulated secretion in neuronal and endocrine contexts, shaping neurotransmitter and hormone release dynamics. STXBP5-linked modulation of vesicular trafficking has been studied in pathways governing synaptic transmission, platelet granule release, and insulin secretion, connecting its activity to cardiometabolic and neurobiological phenotypes. Altered tomosyn expression or function can perturb secretion-dependent signaling networks, making STXBP5 a useful node for investigating dysregulated vesicle fusion in disease-relevant cellular models.
Tomosyn CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous STXBP5 expression without altering the underlying DNA sequence.
Tomosyn CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the STXBP5 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 STXBP5 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Tomosyn expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native STXBP5 locus and enabling the study of Tomosyn-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Tomosyn pathway restoration in tumor cells with silenced or reduced STXBP5 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.