Date published: 2026-8-6

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alpha 1 Sodium Potassium ATPase/ATP1A1 Lentiviral Activation Particles (m): sc-419236-LAC

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Datasheets
  • Target species: mouse
  • 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
  • alpha 1 Sodium Potassium ATPase/ATP1A1 Lentiviral Activation Particles (m) is a synergistic activation mediator (SAM) transcription activation system designed to specifically and efficiently upregulate gene expression via lentiviral transduction of cells
  • alpha 1 Sodium Potassium ATPase/ATP1A1 Lentiviral Activation Particles (m) contain the following SAM Activation elements: a deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, an MS2-p65-HSF1 fusion protein and a target-specific 20 nt guide RNA. They also contain the blasticidin, hygromycin and puromycin resistance genes
  • Upon transduction, the SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
  • gRNAs encoded by alpha 1 Sodium Potassium ATPase/ATP1A1 Lentiviral Activation Plasmid (m) and alpha 1 Sodium Potassium ATPase/ATP1A1 Lentiviral Activation Plasmid (m2) target distinct regulatory regions of the Atp1a1 promoter. One or both designs may be available
  • Following transfection, gene activation efficiency can be assayed by WB, IF or IHC using antibody: alpha 1 Sodium Potassium ATPase/ATP1A1 Antibody (C464.6): sc-21712
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    Product NameCatalog #UNITPriceQtyFAVORITES

    alpha 1 Sodium Potassium ATPase/ATP1A1 Lentiviral Activation Particles (m)

    sc-419236-LAC
    200 µl
    $455.00

    Mouse Atp1a1 encodes the alpha 1 catalytic subunit of the Na⁺/K⁺-ATPase, a P-type ATPase that uses ATP hydrolysis to maintain transmembrane Na⁺ and K⁺ gradients essential for resting membrane potential, osmotic balance, and secondary active transport. Beyond ion homeostasis, ATP1A1 participates in signaling processes linked to membrane microdomains, including crosstalk with Src-family kinases and downstream MAPK/ERK-related pathways that can influence proliferation and stress responses. Perturbation of Na⁺/K⁺-ATPase function is widely used to interrogate excitability, epithelial transport, and metabolic coupling, and it provides mechanistic entry points into disease-relevant phenotypes such as cardiometabolic dysfunction, neurological excitability disorders, and renal tubular transport defects. In mouse systems, Atp1a1 is also leveraged as a robust marker for plasma membrane integrity and as a determinant of sensitivity to cardiac glycosides in pathway studies.

    alpha 1 Sodium Potassium ATPase/ATP1A1 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 Atp1a1 upregulation across a broader range of human cell types.

    alpha 1 Sodium Potassium ATPase/ATP1A1 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 Atp1a1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous alpha 1 Sodium Potassium ATPase/ATP1A1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Atp1a1 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.