GPR43 Lentiviral Activation Particles (h2): sc-401858-LAC-2

Human FFAR2 (GPR43) encodes a short-chain fatty acid–sensing G protein–coupled receptor that is activated by acetate and propionate to regulate intracellular signaling through Gαi/o- and Gαq-linked pathways, including modulation of cAMP, calcium flux, and downstream MAPK responses. It is prominently expressed in immune and epithelial contexts where it shapes chemotaxis, cytokine programs, and barrier-associated inflammatory processes, linking microbial fermentation metabolites to host immunometabolic regulation. Dysregulated FFAR2 signaling has been implicated in inflammatory and metabolic disease biology, including altered innate immune activation and adipose-associated metabolic homeostasis. Gene editing of FFAR2 supports mechanistic studies of ligand–receptor pharmacology, GPCR signaling bias, microbiome–host metabolic crosstalk, and functional genomics in relevant cell models.

GPR43 Lentiviral Activation Particles (h2) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient FFAR2 upregulation across a broader range of human cell types.

GPR43 Lentiviral Activation Particles (h2) 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 FFAR2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous GPR43 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native FFAR2 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.