G_{β 1} Lentiviral Activation Particles (h2): sc-401901-LAC-2

Human GNB1 encodes the G protein beta 1 (Gβ1) subunit, a core component of heterotrimeric G proteins that forms obligate dimers with Gγ subunits to couple activated GPCRs to downstream effectors. Gβ1-containing complexes coordinate signal propagation across cAMP/PKA, PLCβ–IP3/DAG–PKC, and ion channel regulatory pathways, shaping second messenger dynamics, membrane excitability, and receptor desensitization/internalization. Genetic and functional perturbations of GNB1 are linked to altered neurotransmission and developmental signaling and have been reported in neurodevelopmental disorders and select cancers, supporting its utility for studying GPCR network dysregulation. Gene editing of GNB1 enables mechanistic dissection of Gβγ-dependent signaling, epistasis with GPCR/effector nodes, and phenotype mapping in neuronal, cardiac, and proliferative cell models.

Gβ 1 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 GNB1 upregulation across a broader range of human cell types.

Gβ 1 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 GNB1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Gβ 1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native GNB1 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.