
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ZNF71 CRISPR Activation Plasmid (h) | sc-410081-ACT | 20 µg | $397.00 |
ZNF71 encodes a KRAB domain–containing C2H2 zinc finger protein implicated in sequence-specific transcriptional regulation and epigenetic control of gene expression. As a putative transcriptional repressor, ZNF71 is expected to interface with KRAB/KAP1 (TRIM28)-associated chromatin remodeling machinery, influencing heterochromatin formation and transcriptional silencing programs that shape cell identity and stress-responsive transcriptional states. Altered regulation of zinc finger transcription factors is frequently linked to dysregulated differentiation, genomic stability, and oncogenic transcriptional networks, making ZNF71 pertinent to studies of gene regulatory circuitry. In human systems, investigating ZNF71 expression and downstream transcriptional effects supports mechanistic work on chromatin-dependent pathway modulation and disease-associated transcriptional signatures.
ZNF71 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ZNF71 expression without altering the underlying DNA sequence.
ZNF71 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ZNF71 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 ZNF71 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ZNF71 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ZNF71 locus and enabling the study of ZNF71-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ZNF71 pathway restoration in tumor cells with silenced or reduced ZNF71 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.