
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Pannexin-1 Lentiviral Activation Particles (m) | sc-424967-LAC | 200 µl | $455.00 |
Panx1 encodes pannexin-1, a widely expressed plasma membrane channel that enables regulated release of ATP and other small molecules to support paracrine signaling. Pannexin-1 activity integrates with purinergic (P2X/P2Y) receptor pathways to shape calcium flux, inflammasome-associated signaling, and coordinated cellular responses during stress, mechanical stimulation, and cell death. In mouse systems, Panx1 has been implicated in modulation of immune cell recruitment and cytokine networks, as well as regulation of neuronal and glial communication through extracellular nucleotide signaling. Dysregulated PANX1 channel function and altered ATP release dynamics are frequently studied in contexts including neuroinflammation, neuropathic pain, ischemic injury responses, and tumor–immune interactions as mechanistic research targets.
Pannexin-1 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 Panx1 upregulation across a broader range of human cell types.
Pannexin-1 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 Panx1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Pannexin-1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Panx1 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.