beta 3 Sodium Potassium ATPase/ATP1B3 Lentiviral Activation Particles (m): sc-419239-LAC

Atp1b3 encodes the β3 subunit of the Na⁺/K⁺-ATPase, an essential plasma membrane enzyme complex that maintains electrochemical Na⁺ and K⁺ gradients required for membrane potential, osmotic homeostasis, and secondary active transport. By supporting ion-dependent processes, ATP1B3 influences cellular excitability, nutrient uptake, volume regulation, and signaling pathways linked to epithelial polarity and immune cell activation. Altered Na⁺/K⁺-ATPase subunit composition or expression has been associated with disrupted barrier function, aberrant inflammatory signaling, and stress responses that are relevant to cardiovascular, neurological, and metabolic disease biology. In mouse models, modulating Atp1b3 expression can help dissect how ion transport machinery coordinates tissue physiology and responses to injury or inflammation.

beta 3 Sodium Potassium ATPase/ATP1B3 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 Atp1b3 upregulation across a broader range of human cell types.

beta 3 Sodium Potassium ATPase/ATP1B3 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 Atp1b3 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous beta 3 Sodium Potassium ATPase/ATP1B3 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Atp1b3 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.