
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FEZF2 CRISPR Activation Plasmid (h) | sc-406571-ACT | 20 µg | $397.00 |
FEZF2 (FEZ family zinc finger 2) encodes a transcription factor that plays a central role in neurodevelopment by directing cortical projection neuron identity and regulating programs for neuronal differentiation, axon guidance, and corticothalamic connectivity. Through its zinc finger DNA-binding domains, FEZF2 coordinates gene regulatory networks that shape forebrain patterning and maturation of excitatory neuronal lineages, interfacing with developmental signaling and chromatin-dependent transcriptional control. Altered FEZF2 regulation has been associated with neurodevelopmental phenotypes and is studied in the context of dysregulated neuronal circuit formation relevant to complex brain disorders.
FEZF2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous FEZF2 expression without altering the underlying DNA sequence.
FEZF2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the FEZF2 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 FEZF2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous FEZF2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native FEZF2 locus and enabling the study of FEZF2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of FEZF2 pathway restoration in tumor cells with silenced or reduced FEZF2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.