
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FEZ1 CRISPR Activation Plasmid (h) | sc-404727-ACT | 20 µg | $397.00 |
LZTS1 (also known as FEZ1) encodes a leucine zipper tumor suppressor that contributes to regulation of cell-cycle progression and maintenance of genomic stability. FEZ1 has been linked to microtubule and centrosome-associated processes and can influence checkpoint control and proliferation through interactions with mitotic regulatory machinery. Reduced expression or loss of LZTS1 has been reported across multiple human cancers, where it is associated with dysregulated growth and altered cell-cycle control. These features make FEZ1 a useful model for studying tumor-suppressor pathways, mitotic fidelity, and context-specific transcriptional regulation in human cells.
FEZ1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous LZTS1 expression without altering the underlying DNA sequence.
FEZ1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the LZTS1 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 LZTS1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous FEZ1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native LZTS1 locus and enabling the study of FEZ1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of FEZ1 pathway restoration in tumor cells with silenced or reduced LZTS1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.