
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TBX3 CRISPR Activation Plasmid (h) | sc-400754-ACT | 20 µg | $397.00 | |||
TBX3 CRISPR Activation Plasmid (h2) | sc-400754-ACT-2 | 20 µg | $397.00 |
TBX3 encodes a T-box family transcription factor that regulates developmental patterning, cell fate decisions, and tissue morphogenesis through sequence-specific DNA binding and transcriptional repression or activation. In human cells, TBX3 integrates with growth and differentiation programs, intersecting with pathways controlling proliferation, senescence, epithelial–mesenchymal dynamics, and lineage specification. Dysregulated TBX3 expression has been linked to altered developmental phenotypes and has been studied for roles in oncogenic transcriptional networks that influence cell cycle control and metastatic traits. As a nuclear regulator, TBX3 is commonly investigated using genome engineering and transcriptome profiling to map downstream targets and context-dependent transcriptional programs.
TBX3 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TBX3 expression without altering the underlying DNA sequence.
TBX3 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TBX3 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 TBX3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TBX3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TBX3 locus and enabling the study of TBX3-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TBX3 pathway restoration in tumor cells with silenced or reduced TBX3 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.