PLC γ2 Lentiviral Activation Particles (h): sc-400451-LAC

Human PLCG2 encodes phospholipase Cγ2 (PLCγ2), a signal-transducing enzyme that hydrolyzes PIP2 to generate IP3 and DAG, thereby mobilizing intracellular Ca2+ and activating PKC-dependent programs. PLCγ2 functions downstream of immunoreceptor tyrosine-based signaling and receptor tyrosine kinases, integrating cues from B cell receptor, Fc receptors, and other adaptor-driven complexes to regulate activation, cytokine responses, and cytoskeletal remodeling. Through its roles in calcium flux and MAPK/NF-κB–linked pathways, PLCG2 is central to innate and adaptive immune cell function. Genetic perturbations and dysregulated PLCγ2 signaling have been associated with immune dysregulation and inflammatory phenotypes, making it a relevant node for mechanistic studies of immune signaling networks.

PLC γ2 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 PLCG2 upregulation across a broader range of human cell types.

PLC γ2 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 PLCG2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous PLC γ2 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native PLCG2 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.