
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GI24 Lentiviral Activation Particles (h) | sc-407831-LAC | 200 µl | $455.00 |
VSIR encodes GI24, also known as VISTA, a type I transmembrane immune regulatory protein enriched in myeloid lineages and other antigen-presenting cells. GI24 functions as an immune checkpoint molecule that modulates T cell activation, cytokine output, and peripheral tolerance, shaping inflammatory tone within tissue microenvironments. Its activity is linked to regulation of antigen presentation and downstream signaling programs that influence immune-cell crosstalk, including pathways governing transcriptional responses to inflammatory cues. Altered VSIR expression and GI24-mediated signaling have been associated with immune evasion and dysregulated inflammation in cancer and immune-mediated disease contexts, supporting its utility as a mechanistic node for immunology research.
GI24 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 VSIR upregulation across a broader range of human cell types.
GI24 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 VSIR transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous GI24 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native VSIR 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.