Nicotinic Acetylcholine Receptor alpha 9/CHRNA9 Lentiviral Activation Particles (h): sc-402753-LAC

CHRNA9 encodes the nicotinic acetylcholine receptor alpha 9 subunit, a ligand-gated ion channel component that assembles with partner subunits to mediate acetylcholine-evoked cation flux and downstream Ca2+-dependent signaling. CHRNA9-linked receptor activity influences membrane excitability, synaptic and non-neuronal cholinergic signaling, and modulation of cellular responses through pathways coupled to ion homeostasis and second-messenger cascades. In human tissues, altered CHRNA9 expression or receptor function has been associated with sensory and inflammatory biology and has been studied in the context of cancer-related signaling phenotypes and other disorders involving dysregulated cholinergic pathways. As a result, CHRNA9 is a useful target for dissecting nicotinic receptor subunit composition, stimulus-dependent transcriptional programs, and cell-state transitions driven by cholinergic cues.

Nicotinic Acetylcholine Receptor alpha 9/CHRNA9 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 CHRNA9 upregulation across a broader range of human cell types.

Nicotinic Acetylcholine Receptor alpha 9/CHRNA9 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 CHRNA9 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Nicotinic Acetylcholine Receptor alpha 9/CHRNA9 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native CHRNA9 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.