
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CYP7B1 CRISPR Activation Plasmid (h) | sc-405345-ACT | 20 µg | $397.00 |
Human CYP7B1 encodes cytochrome P450 7B1, a microsomal monooxygenase that catalyzes 7α-hydroxylation of oxysterols and steroid intermediates, supporting bile acid synthesis and sterol hormone metabolism. By modulating levels of signaling-active oxysterols, CYP7B1 influences lipid homeostasis and nuclear receptor–linked transcriptional programs in hepatic and extrahepatic tissues. Dysregulation of CYP7B1 activity is associated with inborn errors of sterol/bile acid metabolism and has been linked to neurological and hepatic phenotypes through altered oxysterol clearance and downstream pathway imbalance. As a result, CYP7B1 is widely studied in contexts including cholesterol turnover, neurosteroid signaling, and metabolic stress responses.
CYP7B1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CYP7B1 expression without altering the underlying DNA sequence.
CYP7B1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CYP7B1 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 CYP7B1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CYP7B1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CYP7B1 locus and enabling the study of CYP7B1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CYP7B1 pathway restoration in tumor cells with silenced or reduced CYP7B1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.