alpha 1 Sodium Potassium ATPase/ATP1A1 CRISPR Activation Plasmid (m): sc-419236-ACT

Atp1a1 encodes the alpha 1 catalytic subunit of the Na⁺/K⁺-ATPase, a plasma membrane P-type ATPase that maintains sodium and potassium gradients essential for membrane potential, osmotic homeostasis, and secondary active transport. By regulating ionic balance, ATP1A1 influences processes including neuronal excitability, epithelial transport, cell volume control, and metabolic coupling to ATP utilization. Na⁺/K⁺-ATPase activity also participates in signal transduction by organizing membrane microdomains and modulating pathways linked to calcium handling and stress responses. Dysregulated ATP1A1 function has been associated with altered excitability and transport phenotypes, making it relevant to studies of neurological function, kidney and airway epithelia, and cellular responses to ionic stress in mouse models.

alpha 1 Sodium Potassium ATPase/ATP1A1 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Atp1a1 expression without altering the underlying DNA sequence.

alpha 1 Sodium Potassium ATPase/ATP1A1 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Atp1a1 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 Atp1a1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous alpha 1 Sodium Potassium ATPase/ATP1A1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Atp1a1 locus and enabling the study of alpha 1 Sodium Potassium ATPase/ATP1A1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of alpha 1 Sodium Potassium ATPase/ATP1A1 pathway restoration in tumor cells with silenced or reduced Atp1a1 expression.

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