
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Neuregulin-1/NRG1 Lentiviral Activation Particles (m) | sc-431734-LAC | 200 µl | $455.00 |
Mouse Nrg1 encodes Neuregulin-1 (NRG1), an EGF-like growth factor that signals primarily through ERBB3/ERBB4 receptor tyrosine kinases to activate PI3K–AKT, MAPK/ERK, and related downstream programs. NRG1–ERBB signaling regulates cell fate decisions, proliferation, migration, and survival, with prominent roles in neuronal development, synaptic plasticity, and myelination via neuron–glia communication. In peripheral tissues, NRG1 contributes to epithelial and cardiac biology by shaping differentiation and stress-responsive signaling. Dysregulated NRG1 expression or signaling has been associated with neurodevelopmental and neuropsychiatric phenotypes, demyelinating processes, and oncogenic pathway activation, motivating mechanistic studies in mouse models.
Neuregulin-1/NRG1 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 Nrg1 upregulation across a broader range of human cell types.
Neuregulin-1/NRG1 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 Nrg1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Neuregulin-1/NRG1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Nrg1 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.