GPR35 Lentiviral Activation Particles (m): sc-425672-LAC
- Target species: mouse
- 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
- GPR35 Lentiviral Activation Particles (m) is a synergistic activation mediator (SAM) transcription activation system designed to specifically and efficiently upregulate gene expression via lentiviral transduction of cells
- GPR35 Lentiviral Activation Particles (m) contain the following SAM Activation elements: a deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, an MS2-p65-HSF1 fusion protein and a target-specific 20 nt guide RNA. They also contain the blasticidin, hygromycin and puromycin resistance genes
- Upon transduction, the SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by GPR35 Lentiviral Activation Plasmid (m) and GPR35 Lentiviral Activation Plasmid (m2) target distinct regulatory regions of the Gpr35 promoter. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GPR35 Lentiviral Activation Particles (m) | sc-425672-LAC | 200 µl | $455.00 |
Mouse Gpr35 encodes GPR35, a rhodopsin-like G protein–coupled receptor implicated in sensing small-molecule ligands and shaping intracellular signaling outputs that influence calcium flux, cAMP dynamics, and downstream transcriptional programs. GPR35 activity has been linked to regulation of immune cell chemotaxis and activation, epithelial barrier responses, and broader inflammatory signaling networks, including pathways that intersect with MAPK and NF-κB-dependent gene expression. Expression and genetic associations for GPR35 have been reported in tissues relevant to mucosal immunity and metabolic homeostasis, motivating investigation in models of intestinal inflammation, pain signaling, and cardiometabolic phenotypes. As a conserved GPCR with context-dependent coupling, GPR35 provides a tractable node for dissecting receptor-driven gene regulatory programs in primary cells and disease-relevant mouse systems.
GPR35 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 Gpr35 upregulation across a broader range of human cell types.
GPR35 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 Gpr35 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous GPR35 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Gpr35 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.