
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
NPAS4 Lentiviral Activation Particles (m) | sc-432569-LAC | 200 µl | $455.00 |
Mouse Npas4 encodes NPAS4, an activity-dependent bHLH-PAS transcription factor that couples neuronal excitation to gene programs controlling inhibitory synapse development and excitation–inhibition balance. NPAS4 is induced by calcium signaling and participates in transcriptional networks that shape synaptic plasticity, circuit refinement, and homeostatic responses to altered neuronal activity. Through regulation of downstream targets linked to GABAergic synapse modulation and stimulus-dependent transcription, NPAS4 influences stress responsivity, learning-related plasticity, and metabolic adaptation in neural tissues. Dysregulated NPAS4-associated pathways have been studied in the context of neuropsychiatric and neurodegenerative disease mechanisms, including altered network excitability and impaired cognitive function.
NPAS4 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 Npas4 upregulation across a broader range of human cell types.
NPAS4 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 Npas4 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous NPAS4 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Npas4 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.