TGF beta Receptor 2/TGFBR2 CRISPR Activation Plasmid (h): sc-400144-ACT

TGFBR2 encodes the type II receptor for transforming growth factor beta (TGF-β), a transmembrane serine/threonine kinase that initiates canonical SMAD2/3 signaling upon ligand binding and receptor complex formation with type I receptors. Through these pathways, TGFBR2 regulates cell-cycle control, differentiation, apoptosis, immune modulation, and extracellular matrix remodeling, and it also intersects with non-canonical signaling such as MAPK, PI3K/AKT, and Rho-family GTPases. Dysregulated TGF-β/TGFBR2 signaling is implicated in fibrosis, altered immune surveillance, epithelial–mesenchymal transition, and tumor microenvironment biology, while loss-of-function variants are linked to aberrant tissue homeostasis and cancer-associated signaling rewiring. As a consequence, TGFBR2 serves as a key node for studying context-dependent growth inhibition versus pro-migratory and pro-fibrotic transcriptional programs.

TGF beta Receptor 2/TGFBR2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TGFBR2 expression without altering the underlying DNA sequence.

TGF beta Receptor 2/TGFBR2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TGFBR2 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 TGFBR2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TGF beta Receptor 2/TGFBR2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TGFBR2 locus and enabling the study of TGF beta Receptor 2/TGFBR2-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 2/TGFBR2 pathway restoration in tumor cells with silenced or reduced TGFBR2 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.