
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
N4BP2 Lentiviral Activation Particles (h) | sc-412585-LAC | 200 µl | $455.00 |
N4BP2 (NEDD4 binding protein 2) encodes a large intracellular protein implicated in ubiquitin-dependent signaling through interactions with NEDD4-family E3 ubiquitin ligases. Reported functions link N4BP2 to regulation of protein turnover and trafficking, with downstream effects on cellular homeostasis, stress responses, and signal transduction networks that depend on controlled ubiquitination. In immune and hematopoietic contexts, N4BP2 expression has been associated with modulation of inflammatory signaling and RNA/protein regulatory processes, suggesting roles in shaping cell-state transitions. Dysregulated ubiquitin pathway components, including NEDD4-interacting factors such as N4BP2, are frequently examined for associations with cancer biology, neurobiology, and immune-related disease mechanisms.
N4BP2 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 N4BP2 upregulation across a broader range of human cell types.
N4BP2 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 N4BP2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous N4BP2 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native N4BP2 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.