
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
fetuin-B CRISPR Activation Plasmid (h) | sc-405331-ACT | 20 µg | $397.00 |
Human FETUB encodes fetuin-B, a secreted glycoprotein of the cystatin superfamily that circulates in plasma and modulates extracellular protease activity, including inhibition of metalloproteinases such as ovastacin. By regulating proteolysis in the pericellular space, fetuin-B contributes to homeostatic control of tissue remodeling and protease-driven signaling processes. FETUB expression is enriched in liver and is linked to metabolic and inflammatory physiology, making it relevant for studies of protease regulation, secreted factor biology, and biomarker-associated disease mechanisms.
fetuin-B CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous FETUB expression without altering the underlying DNA sequence.
fetuin-B CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the FETUB 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 FETUB transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous fetuin-B expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native FETUB locus and enabling the study of fetuin-B-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of fetuin-B pathway restoration in tumor cells with silenced or reduced FETUB expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.