
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Na+ CP type Xα Lentiviral Activation Particles (h) | sc-407011-LAC | 200 µl | $455.00 |
SCN10A encodes the voltage-gated sodium channel Na+ CP type Xα (NaV1.8), a pore-forming α subunit that supports tetrodotoxin-resistant sodium influx and repetitive firing in excitable cells. By shaping action potential initiation and propagation, this channel contributes to membrane excitability programs that intersect with nociceptive signaling, neuroimmune crosstalk, and activity-dependent transcriptional responses. Human genetic variation in SCN10A has been associated with cardiac conduction traits and arrhythmia susceptibility, and altered NaV1.8 activity has been linked to pain-related neurophysiology and inflammatory hypersensitivity. These properties make SCN10A a useful target for investigating sodium channel biophysics, excitability-driven signaling pathways, and genotype–phenotype relationships in neuronal and cardiac model systems.
Na+ CP type Xα 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 SCN10A upregulation across a broader range of human cell types.
Na+ CP type Xα 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 SCN10A transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Na+ CP type Xα expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native SCN10A 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.