Date published: 2026-8-29

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NCX2 CRISPR Activation Plasmid (h): sc-403352-ACT

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • NCX2 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
  • NCX2 CRISPR Activation Plasmid (h) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
  • The resulting 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 NCX2 CRISPR Activation Plasmid (h) and NCX2 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the SLC8A2 transcriptional start site. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: NCX2 Antibody (E-1): sc-515768
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    NCX2 CRISPR Activation Plasmid (h)

    sc-403352-ACT
    20 µg
    $397.00

    SLC8A2 encodes the human Na⁺/Ca²⁺ exchanger NCX2, a plasma membrane antiporter that couples the Na⁺ gradient to Ca²⁺ extrusion or, under specific electrochemical conditions, Ca²⁺ entry. By shaping cytosolic Ca²⁺ dynamics, NCX2 influences activity-dependent signaling, membrane excitability, and Ca²⁺-dependent enzyme activation, integrating with pathways that regulate synaptic transmission and neuronal homeostasis. Altered sodium–calcium exchange can perturb Ca²⁺ handling and cellular resilience to ionic stress, making SLC8A2 a relevant target for studying mechanisms linked to neurological dysfunction and neurodegeneration. Its neuron-enriched expression profile also supports investigations into region- and cell-type-specific Ca²⁺ regulation in human model systems.

    NCX2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SLC8A2 expression without altering the underlying DNA sequence.

    NCX2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SLC8A2 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 SLC8A2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous NCX2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SLC8A2 locus and enabling the study of NCX2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of NCX2 pathway restoration in tumor cells with silenced or reduced SLC8A2 expression.

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