Date published: 2026-7-14

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UTX CRISPR Activation Plasmid (h): sc-402761-ACT

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • UTX CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
  • UTX 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 UTX CRISPR Activation Plasmid (h) and UTX CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the KDM6A 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: UTX Antibody (E-8): sc-514859
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    UTX CRISPR Activation Plasmid (h)

    sc-402761-ACT
    20 µg
    $397.00

    UTX CRISPR Activation Plasmid (h2)

    sc-402761-ACT-2
    20 µg
    $397.00

    Human KDM6A encodes UTX, a Jumonji C (JmjC) domain–containing histone demethylase that catalyzes removal of H3K27me3, counteracting Polycomb-mediated repression to promote transcriptional competence. UTX operates within chromatin-remodeling networks, including functional coupling to COMPASS/MLL-associated H3K4 methylation and regulation of lineage-specifying gene programs. Through these activities, KDM6A influences cell cycle control, differentiation, and epigenetic state maintenance across multiple cell types. Altered KDM6A/UTX function is frequently studied in the context of dysregulated epigenetic landscapes observed in cancer biology and developmental disorders.

    UTX CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous KDM6A expression without altering the underlying DNA sequence.

    UTX CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the KDM6A 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 KDM6A transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous UTX expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native KDM6A locus and enabling the study of UTX-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of UTX pathway restoration in tumor cells with silenced or reduced KDM6A expression.

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