Adenylate cyclase 3/AC3/ADCY3 Lentiviral Activation Particles (m): sc-430515-LAC

Mouse Adcy3 encodes adenylate cyclase 3 (AC3/ADCY3), a membrane-associated enzyme that converts ATP to cyclic AMP, thereby coupling GPCR signaling to downstream PKA- and CREB-dependent transcriptional programs. AC3 contributes to sensory and neuroendocrine signaling, including olfactory transduction and cAMP-regulated control of cellular metabolism and differentiation. By shaping compartmentalized cAMP dynamics, ADCY3 influences processes such as neuronal excitability, hormone response pathways, and energy homeostasis. Dysregulated ADCY3-linked signaling has been associated with metabolic phenotypes and neurobehavioral traits in genetic and functional studies, supporting its relevance in models of obesity, insulin sensitivity, and sensory dysfunction.

Adenylate cyclase 3/AC3/ADCY3 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 Adcy3 upregulation across a broader range of human cell types.

Adenylate cyclase 3/AC3/ADCY3 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 Adcy3 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Adenylate cyclase 3/AC3/ADCY3 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Adcy3 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.