Trk C Lentiviral Activation Particles (h): sc-400854-LAC

NTRK3 encodes the receptor tyrosine kinase Trk C, a high-affinity receptor for neurotrophin-3 that regulates neuronal survival, differentiation, axon guidance, and synaptic plasticity. Upon ligand binding and autophosphorylation, Trk C engages canonical signaling cascades including MAPK/ERK, PI3K–AKT, and PLCγ–PKC, coordinating transcriptional programs and cytoskeletal dynamics. NTRK3 activity influences neurodevelopmental processes and neural circuit maintenance, and dysregulation of Trk family signaling has been implicated in contexts such as oncogenic pathway rewiring and altered neuronal function. As a pathway node integrating trophic cues with downstream kinase networks, NTRK3 is widely studied in models of neural lineage specification, signal transduction, and disease-associated signaling perturbations.

Trk C 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 NTRK3 upregulation across a broader range of human cell types.

Trk C 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 NTRK3 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Trk C expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native NTRK3 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.