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.
Smad7 CRISPR Activation Plasmid (h): sc-400251-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Smad7 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- Smad7 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 Smad7 CRISPR Activation Plasmid (h) and Smad7 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the SMAD7 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: Smad7 Antibody (B-8): sc-365846
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Smad7 CRISPR Activation Plasmid (h) | sc-400251-ACT | 20 µg | $397.00 | |||
Smad7 CRISPR Activation Plasmid (h2) | sc-400251-ACT-2 | 20 µg | $397.00 |
SMAD7 encodes Smad7, an inhibitory SMAD that functions as a key negative regulator of TGF-β and BMP signaling by interfering with receptor-mediated phosphorylation of R-SMADs and promoting receptor downregulation. Through modulation of SMAD-dependent transcriptional programs, Smad7 influences epithelial–mesenchymal transition, extracellular matrix remodeling, cell-cycle control, and inflammatory signaling crosstalk. Altered SMAD7 expression has been linked to dysregulated fibrotic responses, impaired immune homeostasis, and aberrant growth control in multiple tissue contexts. These pathway connections make SMAD7 a useful target for dissecting feedback regulation within TGF-β/BMP networks and their downstream transcriptional outputs.
Smad7 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SMAD7 expression without altering the underlying DNA sequence.
Smad7 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SMAD7 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 SMAD7 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Smad7 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SMAD7 locus and enabling the study of Smad7-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Smad7 pathway restoration in tumor cells with silenced or reduced SMAD7 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.