
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MTSS1 Lentiviral Activation Particles (h) | sc-404758-LAC | 200 µl | $455.00 |
Human MTSS1 (metastasis suppressor 1), also known as MIM, encodes an I-BAR domain–containing adaptor that couples membrane curvature sensing to actin cytoskeleton remodeling. MTSS1 participates in processes including lamellipodia and filopodia dynamics, endocytosis, and regulation of cell shape and motility through actin-associated signaling networks. It intersects with pathways controlling cytoskeletal organization and receptor-driven signaling, influencing adhesion and migration phenotypes. Dysregulated MTSS1 expression has been linked to altered invasive behavior and progression across multiple tumor contexts, making it a useful node for studying cytoskeleton-dependent disease mechanisms.
MTSS1 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 MTSS1 upregulation across a broader range of human cell types.
MTSS1 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 MTSS1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous MTSS1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native MTSS1 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.