
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TMEM2 Lentiviral Activation Particles (h) | sc-407487-LAC | 200 µl | $455.00 |
TMEM2 encodes a transmembrane hyaluronidase that contributes to extracellular matrix homeostasis by cleaving hyaluronan, thereby influencing pericellular matrix composition, cell adhesion, and migration. Through regulation of hyaluronan turnover, TMEM2 impacts pathways linked to tissue morphogenesis, mechanotransduction, and inflammatory signaling in stromal and epithelial microenvironments. Altered hyaluronan metabolism and extracellular matrix remodeling are implicated in fibrosis, tumor–stroma interactions, and developmental abnormalities, making TMEM2 a relevant target for dissecting matrix-driven phenotypes. TMEM2 expression and activity are therefore commonly studied in contexts such as cell motility, invasion assays, and extracellular matrix–dependent signaling responses.
TMEM2 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 TMEM2 upregulation across a broader range of human cell types.
TMEM2 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 TMEM2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous TMEM2 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native TMEM2 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.