Date published: 2026-10-8

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T1-cadherin CRISPR Activation Plasmid (h): sc-401986-ACT

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • T1-cadherin CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
  • T1-cadherin 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 T1-cadherin CRISPR Activation Plasmid (h) and T1-cadherin CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the CDH9 transcriptional start site. One or both designs may be available
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    T1-cadherin CRISPR Activation Plasmid (h)

    sc-401986-ACT
    20 µg
    $397.00

    CDH9 encodes T1-cadherin, a calcium-dependent cell–cell adhesion molecule of the cadherin superfamily that contributes to tissue patterning and maintenance of intercellular junctions. Through homophilic binding and linkage to cytoskeletal organization, CDH9 influences cell polarity, migration, and neurite outgrowth programs that intersect with developmental signaling and contact-mediated growth control. Altered cadherin expression profiles can shift adhesion versus motility states and remodel local signaling environments, making CDH9 a useful node for studying mechanisms underlying cellular invasion, differentiation, and network formation. In human biology, dysregulated CDH9 has been examined in contexts where adhesion and connectivity are perturbed, including neurodevelopmental and cancer-associated processes.

    T1-cadherin CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CDH9 expression without altering the underlying DNA sequence.

    T1-cadherin CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CDH9 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 CDH9 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous T1-cadherin expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CDH9 locus and enabling the study of T1-cadherin-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of T1-cadherin pathway restoration in tumor cells with silenced or reduced CDH9 expression.

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