
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ZnT-1 Lentiviral Activation Particles (h) | sc-403094-LAC | 200 µl | $455.00 |
Human SLC30A1 encodes ZnT-1, a plasma membrane zinc exporter that protects cells from zinc overload by lowering cytosolic Zn2+ and shaping metal-dependent signaling. By coupling zinc efflux to cellular homeostasis, ZnT-1 influences oxidative stress responses, apoptosis susceptibility, and metallothionein-regulated buffering, with downstream effects on transcriptional programs that depend on zinc-binding proteins. Altered zinc handling and SLC30A1 dysregulation have been associated with neurobiology and excitability-related processes, as well as broader contexts where metal imbalance contributes to cellular injury and inflammation. This makes ZnT-1 a useful entry point for studying zinc-dependent regulation of membrane physiology and stress-adaptation pathways in human cell models.
ZnT-1 Lentiviral Activation Particles (h) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient SLC30A1 upregulation across a broader range of human cell types.
ZnT-1 Lentiviral Activation Particles (h) deliver all functional components of the synergistic activation mediator (SAM) system via lentiviral transduction. The system comprises three particle preparations co-transduced into target cells: one encoding catalytically inactive dCas9 (D10A and N863A mutations) fused to the VP64 transactivation domain with a blasticidin resistance gene; one encoding the MS2-p65-HSF1 fusion protein with a hygromycin resistance gene; and one encoding a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers with a puromycin resistance gene. Following lentiviral transduction and genomic integration of the expression cassettes, the SAM components are stably expressed and assemble at the target locus within the proximal promoter region upstream of the SLC30A1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous ZnT-1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native SLC30A1 genomic locus and regulatory architecture.
The lentiviral format offers several practical advantages: stable genomic integration supports heritable activation across cell divisions; high-titer particle preparations eliminate the need for in-house viral production; and compatibility with primary, non-dividing, and transfection-resistant cell types expands experimental accessibility. Successful transduction can be confirmed and enriched through triple antibiotic selection using puromycin, hygromycin, and blasticidin.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.