
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DCST2 Lentiviral Activation Particles (h) | sc-405719-LAC | 200 µl | $455.00 | |||
DCST2 Lentiviral Activation Particles (h2) | sc-405719-LAC-2 | 200 µl | $455.00 |
DCST2 (DC-STAMP domain containing 2) encodes a multi-pass membrane protein implicated in cell–cell fusion and membrane remodeling processes, with strongest functional evidence in reproductive biology where DCST family members contribute to sperm–egg fusion competence. As a putative tetraspan-like factor, DCST2 is studied in the context of gamete interaction, membrane trafficking, and surface receptor organization that coordinate fertilization-related signaling and fusion events. Altered regulation of fusion-associated membrane proteins can influence fertility phenotypes and may intersect with pathways controlling cell adhesion and membrane dynamics relevant to developmental biology.
DCST2 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 DCST2 upregulation across a broader range of human cell types.
DCST2 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 DCST2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous DCST2 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native DCST2 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.