
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BCAP Lentiviral Activation Particles (m) | sc-429913-LAC | 200 µl | $455.00 |
Mouse Pik3ap1 encodes B cell adaptor for PI3K (BCAP), a cytosolic signaling scaffold that couples antigen receptor and innate immune receptor inputs to phosphoinositide 3-kinase activation. BCAP helps integrate cues from the B cell receptor, TLRs, and cytokine receptors to modulate PI3K–AKT signaling, downstream MAPK activity, and transcriptional programs that shape proliferation, survival, and differentiation. In immune cells, BCAP influences calcium flux, metabolic reprogramming, and cytoskeletal dynamics that support activation and migration. Dysregulated PI3K pathway signaling and altered adaptor function are relevant to studies of inflammation, autoimmunity, and hematologic malignancy biology where signaling thresholds and lineage fate decisions are perturbed.
BCAP 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 Pik3ap1 upregulation across a broader range of human cell types.
BCAP 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 Pik3ap1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous BCAP expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Pik3ap1 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.