
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GPSM3 Lentiviral Activation Particles (m) | sc-430655-LAC | 200 µl | $455.00 |
Mouse Gpsm3 encodes GPSM3, a GoLoco motif–containing regulator of heterotrimeric G protein signaling that binds GDP-loaded Gα subunits and modulates receptor-driven signal propagation. By tuning Gαi-dependent pathways, GPSM3 influences downstream second-messenger dynamics and integrates inputs from chemokine and other GPCR networks that control leukocyte migration and activation. Expression of GPSM3 is enriched in immune cell lineages, linking it to inflammatory signaling programs and innate immune homeostasis. Dysregulated GPSM3-associated signaling has been investigated in the context of immune-mediated disease mechanisms, making it a useful target for dissecting GPCR–G protein circuitry in mouse models.
GPSM3 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 Gpsm3 upregulation across a broader range of human cell types.
GPSM3 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 Gpsm3 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous GPSM3 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Gpsm3 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.