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 Lentiviral Activation Particles (h): sc-400153-LAC
- Target species: human
- 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
- TGF beta Receptor 1/TGFBR1 Lentiviral Activation Particles (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically and efficiently upregulate gene expression via lentiviral transduction of cells
- TGF beta Receptor 1/TGFBR1 Lentiviral Activation Particles (h) contain the following SAM Activation elements: a deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, an MS2-p65-HSF1 fusion protein and a target-specific 20 nt guide RNA. They also contain the blasticidin, hygromycin and puromycin resistance genes
- Upon transduction, the 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 Lentiviral Activation Plasmid (h) and TGF beta Receptor 1/TGFBR1 Lentiviral Activation Plasmid (h2) target distinct regulatory regions of the TGFBR1 promoter. One or both designs may be available
- Following transfection, gene activation 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 Lentiviral Activation Particles (h) | sc-400153-LAC | 200 µl | $455.00 | |||
TGF beta Receptor 1/TGFBR1 Lentiviral Activation Particles (h2) | sc-400153-LAC-2 | 200 µl | $455.00 |
TGFBR1 encodes transforming growth factor beta receptor 1 (TGF-βRI/ALK5), a serine/threonine kinase that transduces TGF-β ligands into intracellular signaling programs controlling proliferation, differentiation, extracellular matrix remodeling, and immune modulation. Upon ligand engagement with TGFBR2, TGFBR1 is activated to phosphorylate SMAD2/3 and coordinate canonical SMAD4-dependent transcription, while also engaging non-canonical pathways such as MAPK, PI3K/AKT, and Rho-like GTPase signaling. These pathways regulate epithelial–mesenchymal transition, fibroblast activation, and cell cycle checkpoints, making TGFBR1 a central node in tissue homeostasis. Dysregulated TGFBR1 signaling is implicated in fibrosis and diverse cancers, and is also linked to hereditary connective tissue and vascular disorders through altered TGF-β pathway control.
TGF beta Receptor 1/TGFBR1 Lentiviral Activation Particles (h) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient TGFBR1 upregulation across a broader range of human cell types.
TGF beta Receptor 1/TGFBR1 Lentiviral Activation Particles (h) deliver all functional components of the synergistic activation mediator (SAM) system via lentiviral transduction. The system comprises three particle preparations co-transduced into target cells: one encoding catalytically inactive dCas9 (D10A and N863A mutations) fused to the VP64 transactivation domain with a blasticidin resistance gene; one encoding the MS2-p65-HSF1 fusion protein with a hygromycin resistance gene; and one encoding a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers with a puromycin resistance gene. Following lentiviral transduction and genomic integration of the expression cassettes, the SAM components are stably expressed and assemble at the target locus within the proximal promoter region upstream of the TGFBR1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous TGF beta Receptor 1/TGFBR1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native TGFBR1 genomic locus and regulatory architecture.
The lentiviral format offers several practical advantages: stable genomic integration supports heritable activation across cell divisions; high-titer particle preparations eliminate the need for in-house viral production; and compatibility with primary, non-dividing, and transfection-resistant cell types expands experimental accessibility. Successful transduction can be confirmed and enriched through triple antibiotic selection using puromycin, hygromycin, and blasticidin.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.