NT-3 Lentiviral Activation Particles (h): sc-401458-LAC

Neurotrophin 3 (NTF3) encodes NT-3, a secreted neurotrophic factor essential for neuronal survival, differentiation, and synaptic maturation during development and in adult tissue maintenance. NT-3 signals primarily through the TRKC/NTRK3 receptor tyrosine kinase, engaging MAPK/ERK, PI3K–AKT, and PLCγ cascades to regulate neurite outgrowth, neurotransmission, and activity-dependent plasticity. Beyond the nervous system, NT-3 influences sensory neuron–target interactions and can modulate glial and peripheral tissue responses through neurotrophin receptor signaling networks. Dysregulated NTF3/NT-3 pathway activity has been implicated in neurodevelopmental and neurodegenerative phenotypes and is frequently studied in the context of NTRK-mediated signaling alterations relevant to nervous system disorders.

NT-3 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 NTF3 upregulation across a broader range of human cell types.

NT-3 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 NTF3 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous NT-3 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native NTF3 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.