Date published: 2026-8-14

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PXDN CRISPR Activation Plasmid (h): sc-404707-ACT

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • PXDN CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
  • PXDN 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 PXDN CRISPR Activation Plasmid (h) and PXDN CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the PXDN 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: PXDN Antibody (2C11): sc-293408
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    PXDN CRISPR Activation Plasmid (h)

    sc-404707-ACT
    20 µg
    $397.00

    PXDN CRISPR Activation Plasmid (h2)

    sc-404707-ACT-2
    20 µg
    $397.00

    Human PXDN encodes peroxidasin, a secreted extracellular matrix (ECM) heme peroxidase that catalyzes sulfilimine crosslinks in collagen IV, supporting basement membrane assembly and tissue integrity. Through oxidative enzymatic activity and ECM remodeling, PXDN influences cell–matrix adhesion, migration, and vascular and epithelial barrier function. Dysregulated PXDN expression or activity has been linked to developmental and ocular phenotypes and has been investigated in contexts of fibrosis, inflammation, and tumor microenvironment remodeling. As an ECM-associated redox enzyme, PXDN is a useful node for studying basement membrane dynamics and oxidative signaling in cell and organoid models.

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

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

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