TGF beta Receptor 3/TGFBR3 CRISPR Activation Plasmid (h2): sc-401316-ACT-2

Human TGFBR3 (TGF‑β receptor type III; betaglycan) is a membrane proteoglycan that functions as a co-receptor regulating ligand presentation and signaling specificity within the TGF‑β superfamily, including TGF‑βs and select BMPs. By modulating receptor complex assembly and ligand availability at the cell surface, TGFBR3 influences SMAD-dependent transcriptional programs as well as non-canonical pathways linked to epithelial–mesenchymal transition, extracellular matrix remodeling, and cell migration. Altered TGFBR3 expression or shedding has been implicated in dysregulated TGF‑β signaling observed across fibrosis and cancer-associated microenvironmental changes, making it a useful target for mechanistic studies. Reagents for TGFBR3 enable investigations of pathway crosstalk, receptor trafficking and ectodomain shedding, and cell-context-specific responses in human cell models.

TGF beta Receptor 3/TGFBR3 CRISPR Activation Plasmid (h2) provides a targeted, non-destructive approach to upregulating endogenous TGFBR3 expression without altering the underlying DNA sequence.

TGF beta Receptor 3/TGFBR3 CRISPR Activation Plasmid (h2) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TGFBR3 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 TGFBR3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TGF beta Receptor 3/TGFBR3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TGFBR3 locus and enabling the study of TGF beta Receptor 3/TGFBR3-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 3/TGFBR3 pathway restoration in tumor cells with silenced or reduced TGFBR3 expression.

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