Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
WT1 CRISPR Activation Plasmid (h): sc-400095-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- WT1 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- WT1 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 WT1 CRISPR Activation Plasmid (h) and WT1 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the WT1 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: WT1 Antibody (H-1): sc-393498
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
WT1 CRISPR Activation Plasmid (h) | sc-400095-ACT | 20 µg | $397.00 | |||
WT1 CRISPR Activation Plasmid (h2) | sc-400095-ACT-2 | 20 µg | $397.00 |
WT1 (Wilms tumor 1) encodes a zinc-finger transcription factor that regulates cell fate decisions during embryonic development and tissue homeostasis, with prominent roles in nephrogenesis, gonad development, and mesothelial differentiation. WT1 modulates transcriptional programs controlling proliferation, apoptosis, epithelial–mesenchymal transitions, and lineage specification, interfacing with pathways such as Wnt/β-catenin, TGF-β signaling, and growth factor–responsive networks. In human biology, altered WT1 expression or mutation has been linked to developmental disorders and diverse cancer contexts where it can function in a context-dependent manner as a transcriptional regulator of oncogenic or tumor-suppressive gene sets. These features make WT1 a useful node for studying transcriptional network rewiring, differentiation trajectories, and stress-responsive gene regulation.
WT1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous WT1 expression without altering the underlying DNA sequence.
WT1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the WT1 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 WT1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous WT1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native WT1 locus and enabling the study of WT1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of WT1 pathway restoration in tumor cells with silenced or reduced WT1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.