
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
UHRF1 CRISPR Activation Plasmid (m) | sc-421937-ACT | 20 µg | $397.00 |
Mouse Uhrf1 encodes UHRF1, a multidomain epigenetic regulator that recognizes hemimethylated DNA and histone marks to coordinate maintenance DNA methylation during S phase. By recruiting DNMT1 and interacting with chromatin-modifying enzymes, UHRF1 helps preserve genome-wide methylation patterns, supports heterochromatin integrity, and influences replication-coupled chromatin assembly. These activities connect UHRF1 to cell-cycle control, DNA damage responses, and transcriptional programs governing proliferation and differentiation. Dysregulated UHRF1 expression and aberrant DNA methylation landscapes are frequently associated with oncogenic transcriptional reprogramming and genomic instability, making Uhrf1 a key node for studying epigenetic disease mechanisms.
UHRF1 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Uhrf1 expression without altering the underlying DNA sequence.
UHRF1 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Uhrf1 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 Uhrf1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous UHRF1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Uhrf1 locus and enabling the study of UHRF1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of UHRF1 pathway restoration in tumor cells with silenced or reduced Uhrf1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.