
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RANK Lentiviral Activation Particles (m) | sc-423439-LAC | 200 µl | $455.00 |
Mouse Tnfrsf11a encodes RANK, a TNF receptor superfamily member that functions as the cognate receptor for RANKL (TNFSF11) and a central regulator of osteoclast differentiation, activation, and survival. RANK signaling engages TRAF adaptors to activate NF-κB, MAPK, and AP-1 pathways, coordinating bone remodeling and coupling immune cues to skeletal homeostasis. Beyond bone, RANK contributes to immune cell communication and tissue remodeling programs, making it relevant to studies of inflammatory bone loss, osteoclast-driven pathology, and osteoimmunology mechanisms. Dysregulated RANK/RANKL/OPG axis activity is frequently investigated in contexts of altered bone density and pathological resorption in mouse models.
RANK 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 Tnfrsf11a upregulation across a broader range of human cell types.
RANK 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 Tnfrsf11a transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous RANK expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Tnfrsf11a 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.