
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PBEF Lentiviral Activation Particles (m) | sc-425569-LAC | 200 µl | $455.00 |
Mouse Nampt, also known as PBEF/visfatin, encodes nicotinamide phosphoribosyltransferase, the rate-limiting enzyme of the NAD salvage pathway that converts nicotinamide to NMN to sustain cellular NAD pools. By controlling NAD availability, NAMPT modulates sirtuin and PARP-dependent programs that influence mitochondrial metabolism, oxidative stress responses, DNA repair, and inflammatory signaling. NAMPT activity links nutrient sensing to transcriptional and epigenetic regulation, impacting processes such as immune cell activation, adipose biology, and cellular stress adaptation. Dysregulated NAMPT/NAD metabolism has been associated with metabolic dysfunction, neuroinflammatory states, and tumor cell bioenergetic rewiring, making it a useful node for mechanistic studies in mouse models.
PBEF 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 Nampt upregulation across a broader range of human cell types.
PBEF 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 Nampt transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous PBEF expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Nampt 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.