beta 3 Sodium Potassium ATPase/ATP1B3 CRISPR Activation Plasmid (m): sc-419239-ACT

Atp1b3 encodes the β3 subunit of the Na⁺/K⁺-ATPase, a heteromeric P-type ATPase that maintains transmembrane Na⁺ and K⁺ gradients essential for resting membrane potential, osmotic balance, and secondary active transport. By supporting ion homeostasis, ATP1B3 influences processes such as cell volume regulation, epithelial transport, and excitability, and it can modulate signaling networks coupled to membrane potential and ion-dependent kinase activity. The β subunit also contributes to proper assembly, trafficking, and membrane stability of the pump complex, thereby shaping cellular energy demand through ATP-dependent ion transport. Dysregulated Na⁺/K⁺-ATPase function is relevant to models of neurological dysfunction, cardiovascular and renal physiology, and inflammation-associated phenotypes, making Atp1b3 a useful node for mechanistic studies in mouse systems.

beta 3 Sodium Potassium ATPase/ATP1B3 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Atp1b3 expression without altering the underlying DNA sequence.

beta 3 Sodium Potassium ATPase/ATP1B3 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Atp1b3 locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.

Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the Atp1b3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous beta 3 Sodium Potassium ATPase/ATP1B3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Atp1b3 locus and enabling the study of beta 3 Sodium Potassium ATPase/ATP1B3-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of beta 3 Sodium Potassium ATPase/ATP1B3 pathway restoration in tumor cells with silenced or reduced Atp1b3 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.