
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Conductin CRISPR Activation Plasmid (h) | sc-401386-ACT | 20 µg | $397.00 | |||
Conductin CRISPR Activation Plasmid (h2) | sc-401386-ACT-2 | 20 µg | $397.00 |
AXIN2 encodes Conductin, a scaffold protein that functions as a key negative regulator of canonical Wnt/β-catenin signaling by promoting assembly of the β-catenin destruction complex and facilitating β-catenin turnover. As a transcriptional target of Wnt signaling, AXIN2 participates in feedback control of pathway amplitude and duration, influencing cell fate specification, proliferation, and differentiation programs. Dysregulated AXIN2 expression or function is associated with altered Wnt pathway activity implicated in developmental abnormalities and tumor biology, including colorectal and other Wnt-driven malignancies. In human cell models, AXIN2 serves as a readout and modulator of Wnt pathway dynamics relevant to epithelial homeostasis and stem/progenitor cell regulation.
Conductin CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous AXIN2 expression without altering the underlying DNA sequence.
Conductin CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the AXIN2 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 AXIN2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Conductin expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native AXIN2 locus and enabling the study of Conductin-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Conductin pathway restoration in tumor cells with silenced or reduced AXIN2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.