IP3R-III Lentiviral Activation Particles (m): sc-421194-LAC

Itpr3 encodes inositol 1,4,5-trisphosphate receptor type 3 (IP3R-III), an endoplasmic reticulum Ca²⁺ release channel activated downstream of GPCR and receptor tyrosine kinase signaling through PLC-generated IP3. IP3R-III-mediated Ca²⁺ transients regulate processes including secretion, epithelial transport, mitochondrial bioenergetics, and Ca²⁺-dependent gene expression via pathways such as calcineurin–NFAT and CaMK signaling. In mouse tissues, IP3R-III expression is enriched in epithelial and secretory lineages, supporting studies of polarized Ca²⁺ signaling, ER–mitochondria contact sites, and stimulus-coupled calcium oscillations. Dysregulated IP3R-III activity and Ca²⁺ homeostasis have been linked to cellular stress responses and disease-relevant phenotypes involving epithelial dysfunction and aberrant proliferative signaling, making Itpr3 a useful node for mechanistic modeling.

IP3R-III 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 Itpr3 upregulation across a broader range of human cell types.

IP3R-III 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 Itpr3 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous IP3R-III expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Itpr3 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.