
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Herc2 CRISPR Activation Plasmid (m) | sc-420831-ACT | 20 µg | $397.00 | |||
Herc2 CRISPR Activation Plasmid (m2) | sc-420831-ACT-2 | 20 µg | $397.00 |
Mouse HERC2 is a large HECT-type E3 ubiquitin ligase that coordinates ubiquitin-dependent regulation of protein stability and signaling, integrating DNA damage responses with cell-cycle control. It participates in genome maintenance processes including replication stress handling and repair pathway coordination through ubiquitin-mediated modulation of key substrates. HERC2 has also been linked to centrosome function and proteostasis, connecting ubiquitin signaling to chromatin dynamics and cellular homeostasis. Dysregulation of HERC2-associated pathways is relevant to studies of genomic instability phenotypes and neurodevelopmental biology in mammalian model systems.
Herc2 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Herc2 expression without altering the underlying DNA sequence.
Herc2 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Herc2 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 Herc2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Herc2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Herc2 locus and enabling the study of Herc2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Herc2 pathway restoration in tumor cells with silenced or reduced Herc2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.