
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HAI-1 Lentiviral Activation Particles (h) | sc-404011-LAC | 200 µl | $455.00 |
SPINT1 encodes hepatocyte growth factor activator inhibitor type 1 (HAI-1), a membrane-anchored Kunitz-type serine protease inhibitor that restrains pericellular proteolysis at epithelial surfaces. HAI-1 regulates activation of proteases such as matriptase (ST14) and hepsin (HPN), thereby influencing extracellular matrix remodeling, cell–cell junction integrity, and epithelial barrier homeostasis. Through control of protease-dependent processing of growth factors and substrates, SPINT1 modulates signaling axes linked to epithelial differentiation and migratory behavior, including pathways connected to HGF/MET activation. Dysregulated SPINT1/HAI-1 activity has been associated with altered epithelial integrity and protease-driven programs relevant to inflammation and cancer biology.
HAI-1 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 SPINT1 upregulation across a broader range of human cell types.
HAI-1 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 SPINT1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous HAI-1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native SPINT1 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.