
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BIGM103 Lentiviral Activation Particles (m) | sc-426620-LAC | 200 µl | $455.00 |
Slc39a8 encodes the ZIP8 metal ion transporter, which mediates cellular uptake of divalent cations such as manganese and zinc and helps maintain intracellular metal homeostasis. Through regulation of manganese availability, ZIP8 can influence Mn-dependent enzyme activity, including glycosylation pathways and broader metabolic and redox processes that shape cellular stress responses. Altered SLC39A8/ZIP8 function has been linked in the literature to inflammatory signaling, neurodevelopmental phenotypes, and metabolic traits, consistent with the central role of micronutrient transport in tissue physiology. In mouse systems, Slc39a8 is therefore a useful node for studying metal-dependent regulation of signaling and gene expression programs relevant to disease-associated mechanisms.
BIGM103 Lentiviral Activation Particles (m) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient Slc39a8 upregulation across a broader range of human cell types.
BIGM103 Lentiviral Activation Particles (m) 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 Slc39a8 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous BIGM103 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Slc39a8 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.