
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CUL-7 CRISPR Activation Plasmid (h) | sc-404053-ACT | 20 µg | $397.00 |
Human CUL7 encodes cullin-7 (CUL-7), a scaffold component of Cullin-RING E3 ubiquitin ligase complexes that regulate protein turnover and proteostasis. Through ubiquitin-dependent degradation of specific substrates, CUL-7 influences cell cycle progression, DNA damage responses, and signaling pathways controlling growth and stress adaptation. CUL-7 function intersects with cytoskeletal regulation and mitotic control, linking ubiquitin ligase activity to cell proliferation and genome stability. Dysregulated CUL7 activity has been associated with aberrant growth control and tumor biology, making it relevant for mechanistic studies of oncogenic signaling and ubiquitin-pathway dependencies.
CUL-7 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CUL7 expression without altering the underlying DNA sequence.
CUL-7 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CUL7 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 CUL7 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CUL-7 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CUL7 locus and enabling the study of CUL-7-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CUL-7 pathway restoration in tumor cells with silenced or reduced CUL7 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.