
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ZC3H4 CRISPR Activation Plasmid (h) | sc-411693-ACT | 20 µg | $397.00 |
ZC3H4 encodes a zinc finger CCCH-type RNA-binding protein implicated in post-transcriptional regulation, with emerging roles in controlling RNA fate and transcriptional output. Studies link ZC3H4 to nuclear RNA processing and gene expression programs that shape cell-state transitions, including proliferation and differentiation. Through interactions with RNA and regulatory protein complexes, ZC3H4 is positioned to influence pathways governing transcript stability and nuclear surveillance. Dysregulation of RNA-binding and processing factors such as ZC3H4 is frequently associated with altered gene expression signatures observed in cancer and other disorders involving aberrant RNA metabolism.
ZC3H4 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ZC3H4 expression without altering the underlying DNA sequence.
ZC3H4 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ZC3H4 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 ZC3H4 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ZC3H4 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ZC3H4 locus and enabling the study of ZC3H4-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ZC3H4 pathway restoration in tumor cells with silenced or reduced ZC3H4 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.