
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
KiSS-1 CRISPR Activation Plasmid (h) | sc-402710-ACT | 20 µg | $397.00 |
Human KISS1 encodes the KiSS-1 peptide precursor that is proteolytically processed into kisspeptins, secreted ligands for the G protein-coupled receptor KISS1R (GPR54). Kisspeptin–KISS1R signaling activates PLC/PKC-dependent calcium mobilization and MAPK pathways, integrating neuroendocrine control of gonadotropin-releasing hormone release and broader reproductive axis regulation. In addition to endocrine function, KISS1 has been linked to regulation of cell migration and invasion, with context-dependent effects on metastatic behavior across tumor models. Altered KISS1/KISS1R signaling has been associated with reproductive disorders and cancer biology, making it a useful node for studying ligand-receptor signaling and transcriptional regulation.
KiSS-1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous KISS1 expression without altering the underlying DNA sequence.
KiSS-1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the KISS1 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 KISS1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous KiSS-1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native KISS1 locus and enabling the study of KiSS-1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of KiSS-1 pathway restoration in tumor cells with silenced or reduced KISS1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.