
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PSS1 Lentiviral Activation Particles (m) | sc-422474-LAC | 200 µl | $455.00 |
Mouse Ptdss1 encodes phosphatidylserine synthase 1 (PSS1), an endoplasmic reticulum membrane enzyme that catalyzes base-exchange reactions to generate phosphatidylserine from phosphatidylcholine. By controlling phosphatidylserine availability, PSS1 influences membrane biogenesis, lipid asymmetry and signaling, and supports downstream phosphatidylethanolamine synthesis via mitochondrial decarboxylation. This lipid node intersects with pathways regulating vesicle trafficking, apoptosis-associated membrane remodeling, and immunologically relevant “eat-me” signaling. Altered phosphatidylserine metabolism has been linked to neurodevelopmental phenotypes and broader membrane homeostasis disorders, making Ptdss1 a useful target for mechanistic studies of lipid-driven cellular physiology.
PSS1 Lentiviral Activation Particles (m) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient Ptdss1 upregulation across a broader range of human cell types.
PSS1 Lentiviral Activation Particles (m) 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 Ptdss1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous PSS1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Ptdss1 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.