GLP-1R Lentiviral Activation Particles (h): sc-400847-LAC

GLP1R encodes the glucagon-like peptide-1 receptor (GLP-1R), a class B GPCR that couples primarily to Gαs to elevate cAMP and activate PKA/EPAC signaling. Downstream effects include CREB-dependent transcription, modulation of intracellular calcium dynamics, and pathway crosstalk with MAPK/ERK and PI3K/AKT that shapes cell excitability, secretion, and metabolic gene programs. In pancreatic islet biology, GLP-1R signaling amplifies glucose-stimulated insulin secretion and supports β-cell functional responses, while in extra-pancreatic tissues it contributes to neuroendocrine and gastrointestinal signaling. Altered GLP1R expression or signaling has been implicated in metabolic dysregulation phenotypes relevant to diabetes and obesity research, and provides a mechanistic handle for studying cAMP-driven transcriptional control in human cellular systems.

GLP-1R 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 GLP1R upregulation across a broader range of human cell types.

GLP-1R 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 GLP1R transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous GLP-1R expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native GLP1R 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.