
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LIV-1 CRISPR Activation Plasmid (h) | sc-403294-ACT | 20 µg | $397.00 |
SLC39A6 encodes LIV-1 (ZIP6), a plasma membrane zinc transporter that regulates cellular zinc influx and helps maintain metal homeostasis. LIV-1–dependent zinc signaling influences pathways controlling proliferation, differentiation, and motility, including EMT-associated programs and downstream kinase and transcriptional networks. Altered SLC39A6 expression has been reported across multiple tumor contexts and is linked to changes in invasion phenotypes and hormone-responsive signaling, making it a useful node for studying metal-regulated cell-state transitions. In human cell models, LIV-1 provides a mechanistic handle to interrogate how zinc availability reshapes transcriptional circuitry and stress-adaptive responses.
LIV-1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SLC39A6 expression without altering the underlying DNA sequence.
LIV-1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SLC39A6 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 SLC39A6 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous LIV-1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SLC39A6 locus and enabling the study of LIV-1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of LIV-1 pathway restoration in tumor cells with silenced or reduced SLC39A6 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.