
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CRBN CRISPR Activation Plasmid (m) | sc-425519-ACT | 20 µg | $397.00 |
Mouse Crbn encodes cereblon (CRBN), a substrate receptor for the CUL4–DDB1 E3 ubiquitin ligase complex that regulates proteostasis through targeted ubiquitination and degradation of specific client proteins. By controlling the stability of signaling and transcriptional regulators, CRBN influences cell-cycle progression, differentiation, and stress-response pathways, and intersects with broader ubiquitin–proteasome and DNA damage–associated processes. Altered CRBN activity has been implicated in neurodevelopmental phenotypes and immune and metabolic regulation, making Crbn a useful gene for mechanistic studies of protein turnover and pathway rewiring in disease-relevant cellular models.
CRBN CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Crbn expression without altering the underlying DNA sequence.
CRBN CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Crbn 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 Crbn transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CRBN expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Crbn locus and enabling the study of CRBN-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CRBN pathway restoration in tumor cells with silenced or reduced Crbn expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.