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.
Wnt-10b CRISPR Activation Plasmid (h): sc-401465-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Wnt-10b CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- Wnt-10b 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 Wnt-10b CRISPR Activation Plasmid (h) and Wnt-10b CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the WNT10B 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: Wnt-10b Antibody (H-8): sc-518156
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Wnt-10b CRISPR Activation Plasmid (h) | sc-401465-ACT | 20 µg | $397.00 | |||
Wnt-10b CRISPR Activation Plasmid (h2) | sc-401465-ACT-2 | 20 µg | $397.00 |
WNT10B encodes the secreted glycoprotein Wnt-10b, a lipid-modified ligand that activates Frizzled/LRP receptor complexes to regulate canonical Wnt/β-catenin transcriptional programs and context-dependent noncanonical signaling. Wnt-10b influences cell fate decisions, proliferation, and differentiation, with prominent roles in osteogenesis and adipogenesis as well as epithelial and stromal crosstalk during development and tissue remodeling. Dysregulated WNT10B expression or signaling output can perturb β-catenin–dependent gene expression networks and alter pathway cross-talk with TCF/LEF, BMP, and Notch-associated processes. These pathway alterations are frequently investigated in models of aberrant growth control, fibrosis-associated remodeling, and tumor biology where Wnt pathway activity modulates stem-like phenotypes and microenvironmental responses.
Wnt-10b CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous WNT10B expression without altering the underlying DNA sequence.
Wnt-10b CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the WNT10B 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 WNT10B transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Wnt-10b expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native WNT10B locus and enabling the study of Wnt-10b-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Wnt-10b pathway restoration in tumor cells with silenced or reduced WNT10B expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.