
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TPCN1 Lentiviral Activation Particles (h) | sc-404943-LAC | 200 µl | $455.00 |
TPCN1 (two-pore segment channel 1; TPC1) encodes an endolysosomal cation channel that mediates NAADP-dependent Ca²⁺ release from acidic organelles, coordinating local calcium microdomains that shape vesicle trafficking, endosome–lysosome dynamics, and membrane excitability. By coupling ionic flux to organelle membrane potential and pH-dependent signaling, TPCN1 influences processes such as autophagy, endocytic cargo sorting, and receptor recycling. TPCN1 activity intersects with calcium-dependent signaling networks and nutrient-sensing pathways that regulate cellular stress responses and metabolism. Dysregulated endolysosomal calcium handling and trafficking programs linked to TPCN1 are studied in contexts including neurodegeneration, pigmentary and metabolic phenotypes, and cancer-associated invasion and migration.
TPCN1 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 TPCN1 upregulation across a broader range of human cell types.
TPCN1 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 TPCN1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous TPCN1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native TPCN1 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.