
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BMP-3 Lentiviral Activation Particles (m2) | sc-430986-LAC-2 | 200 µl | $455.00 |
Mouse Bmp3 encodes BMP-3, a secreted member of the TGF-β superfamily that functions as an extracellular regulator of osteogenic signaling and skeletal tissue homeostasis. BMP-3 modulates bone formation by influencing BMP/TGF-β pathway activity, including crosstalk with SMAD-dependent transcriptional programs that control osteoblast differentiation and matrix deposition. Genetic and expression studies link altered BMP-3 signaling to variation in bone mineral density and skeletal development phenotypes, supporting its relevance to models of impaired ossification and bone remodeling. Gene editing of Bmp3 in mouse systems enables mechanistic interrogation of skeletal signaling networks, lineage-specific effects in mesenchymal progenitors, and downstream transcriptional and extracellular matrix responses in developmental and disease-relevant contexts.
BMP-3 Lentiviral Activation Particles (m2) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient Bmp3 upregulation across a broader range of human cell types.
BMP-3 Lentiviral Activation Particles (m2) 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 Bmp3 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous BMP-3 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Bmp3 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.