
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Shh Lentiviral Activation Particles (h) | sc-400225-LAC | 200 µl | $455.00 | |||
Shh Lentiviral Activation Particles (h2) | sc-400225-LAC-2 | 200 µl | $455.00 |
Human SHH encodes Sonic hedgehog (Shh), a secreted morphogen that patterns embryonic tissues and regulates cell fate decisions through the Hedgehog signaling cascade. Shh binding to PTCH1 relieves repression of SMO, enabling GLI transcription factor activation and downstream programs controlling proliferation, differentiation, and tissue organization. In adult biology, SHH contributes to stem and progenitor cell maintenance and epithelial–mesenchymal signaling in multiple organs. Aberrant SHH pathway activity has been implicated in developmental malformations and oncogenic signaling contexts, making SHH a central node for mechanistic studies of morphogen gradients and pathway crosstalk.
Shh 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 SHH upregulation across a broader range of human cell types.
Shh 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 SHH transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Shh expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native SHH 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.