
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TGFα CRISPR Activation Plasmid (h) | sc-401563-ACT | 20 µg | $397.00 |
TGFA encodes transforming growth factor alpha (TGFα), a secreted EGFR ligand that stimulates receptor tyrosine kinase signaling to regulate epithelial proliferation, survival, and migration. Upon EGFR engagement, TGFα promotes downstream RAS–RAF–MEK–ERK and PI3K–AKT pathway activity, influencing cell-cycle progression and differentiation programs. Dysregulated TGFA/EGFR signaling is frequently studied in contexts of aberrant growth control and tissue remodeling, with relevance to oncogenic signaling networks and inflammatory microenvironments. As an autocrine/paracrine factor, TGFα is commonly used to interrogate ligand-driven receptor activation, feedback regulation, and pathway crosstalk in human cell models.
TGFα CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TGFA expression without altering the underlying DNA sequence.
TGFα CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TGFA 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 TGFA transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TGFα expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TGFA locus and enabling the study of TGFα-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TGFα pathway restoration in tumor cells with silenced or reduced TGFA expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.