Nicotinic Acetylcholine Receptor alpha 7/CHRNA7 Lentiviral Activation Particles (h): sc-416614-LAC

CHRNA7 encodes the α7 subunit of the nicotinic acetylcholine receptor (nAChR), a homopentameric ligand-gated ion channel with high Ca²⁺ permeability that links cholinergic signaling to rapid membrane depolarization and downstream second-messenger cascades. In neurons and glia, α7 nAChR activity influences synaptic plasticity, neurotransmitter release, and Ca²⁺-dependent pathways including MAPK/ERK and PI3K/AKT signaling, while in immune and epithelial contexts it can modulate cytokine production and cellular excitability. Dysregulated CHRNA7 expression or function has been associated with neuropsychiatric and neurodevelopmental phenotypes, including schizophrenia- and epilepsy-related endophenotypes, and has been investigated in Alzheimer’s disease and inflammatory biology. As a surface receptor integrating ligand binding with intracellular signaling, CHRNA7 is frequently studied in models of neuronal differentiation, network activity, and stimulus-evoked calcium dynamics.

Nicotinic Acetylcholine Receptor alpha 7/CHRNA7 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 CHRNA7 upregulation across a broader range of human cell types.

Nicotinic Acetylcholine Receptor alpha 7/CHRNA7 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 CHRNA7 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 7/CHRNA7 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native CHRNA7 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.