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.
TGF beta Receptor 1/TGFBR1 CRISPR Activation Plasmid (h): sc-400153-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TGF beta Receptor 1/TGFBR1 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- TGF beta Receptor 1/TGFBR1 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 TGF beta Receptor 1/TGFBR1 CRISPR Activation Plasmid (h) and TGF beta Receptor 1/TGFBR1 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the TGFBR1 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: TGF beta Receptor 1/TGFBR1 Antibody (D-1): sc-518018
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TGF beta Receptor 1/TGFBR1 CRISPR Activation Plasmid (h) | sc-400153-ACT | 20 µg | $397.00 | |||
TGF beta Receptor 1/TGFBR1 CRISPR Activation Plasmid (h2) | sc-400153-ACT-2 | 20 µg | $397.00 |
TGFBR1 (TGF beta receptor 1; ALK5) encodes a transmembrane serine/threonine kinase that serves as a core receptor for TGF-β ligands. Upon ligand binding and complex formation with TGFBR2, TGFBR1 propagates canonical SMAD2/3 signaling and intersects with non-canonical MAPK, PI3K/AKT, and Rho-like GTPase pathways to regulate epithelial–mesenchymal transition, extracellular matrix remodeling, cell-cycle control, and immune modulation. Dysregulated TGFBR1 signaling is implicated in fibrosis, aberrant inflammatory responses, and tumor microenvironment biology, where context-dependent changes in pathway output can alter growth control and cell plasticity. As an upstream signaling node, TGFBR1 is widely studied for its role in developmental patterning, tissue homeostasis, and pathway crosstalk that shapes transcriptional programs.
TGF beta Receptor 1/TGFBR1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TGFBR1 expression without altering the underlying DNA sequence.
TGF beta Receptor 1/TGFBR1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TGFBR1 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 TGFBR1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TGF beta Receptor 1/TGFBR1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TGFBR1 locus and enabling the study of TGF beta Receptor 1/TGFBR1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TGF beta Receptor 1/TGFBR1 pathway restoration in tumor cells with silenced or reduced TGFBR1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.