
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ATP11B Lentiviral Activation Particles (h) | sc-411692-LAC | 200 µl | $455.00 |
ATP11B encodes a P4-ATPase phospholipid flippase that helps maintain plasma and organellar membrane lipid asymmetry by translocating aminophospholipids across bilayers in an ATP-dependent manner. Through regulation of membrane composition, ATP11B influences vesicle formation, endosomal trafficking, and recycling processes that intersect with Golgi–endosome transport and broader secretory pathway dynamics. Perturbation of lipid asymmetry and trafficking can impact signaling, cell polarity, and stress responses, making ATP11B relevant to studies of membrane homeostasis and transport-associated phenotypes. Altered ATP11B activity or expression has been examined in the context of disease-relevant cellular behaviors such as drug handling, survival under stress, and changes in intracellular distribution of membrane proteins.
ATP11B 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 ATP11B upregulation across a broader range of human cell types.
ATP11B 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 ATP11B transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous ATP11B expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native ATP11B 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.