GPR4 Lentiviral Activation Particles (m): sc-435597-LAC
- Target species: mouse
- 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
- GPR4 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
- GPR4 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 GPR4 Lentiviral Activation Plasmid (m) and GPR4 Lentiviral Activation Plasmid (m2) target distinct regulatory regions of the Gpr4 promoter. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GPR4 Lentiviral Activation Particles (m) | sc-435597-LAC | 200 µl | $455.00 |
Mouse Gpr4 encodes GPR4, a proton-sensing G protein–coupled receptor that detects extracellular acidification and couples to cAMP and Rho signaling to modulate endothelial and immune cell behavior. GPR4 activation influences vascular tone, barrier function, leukocyte trafficking, and inflammatory gene expression through pathways that can intersect with MAPK and NF-κB-regulated programs. Because tissue acidosis is a common feature of hypoxia and inflammation, GPR4 is frequently studied in contexts such as ischemia-associated stress responses, chronic inflammatory microenvironments, and tumor-associated vascular remodeling. These roles make GPR4 a useful node for dissecting pH-dependent signaling and transcriptional adaptations in mouse models and relevant cell systems.
GPR4 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 Gpr4 upregulation across a broader range of human cell types.
GPR4 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 Gpr4 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous GPR4 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Gpr4 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.