TrkB Lentiviral Activation Particles (h): sc-400142-LAC

NTRK2 encodes the receptor tyrosine kinase TrkB, a high-affinity neurotrophin receptor for BDNF and NT-4/5 that regulates neuronal survival, differentiation, synaptic plasticity, and activity-dependent circuit remodeling. Upon ligand binding, TrkB activates canonical PI3K–AKT, RAS–MAPK/ERK, and PLCγ–Ca2+ signaling cascades, coordinating transcriptional programs and cytoskeletal dynamics that shape neurite outgrowth and synaptic function. Dysregulated NTRK2/TrkB signaling has been linked to altered neurodevelopment and neuropsychiatric phenotypes, and aberrant receptor activity or expression has been studied in cancers with neurotrophin pathway involvement. As a node integrating extracellular neurotrophin cues with intracellular kinase signaling, TrkB is widely used to interrogate pathway crosstalk, neuronal connectivity, and context-specific signaling outputs in human cellular models.

TrkB 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 NTRK2 upregulation across a broader range of human cell types.

TrkB 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 NTRK2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous TrkB expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native NTRK2 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.