
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FKBP10 CRISPR Activation Plasmid (h) | sc-405062-ACT | 20 µg | $397.00 |
FKBP10 encodes FK506-binding protein 10 (FKBP65), an endoplasmic reticulum–resident peptidyl-prolyl cis-trans isomerase that functions as a molecular chaperone during collagen biosynthesis. It supports proper folding, assembly, and maturation of procollagen, influencing extracellular matrix organization and connective tissue homeostasis. FKBP10 activity intersects with ER protein quality control and proteostasis pathways that regulate secretion of collagen-rich matrices. Genetic disruption or dysregulation of FKBP10 is associated with heritable connective tissue and skeletal phenotypes, making it a useful target for studying collagen processing, matrix-driven signaling, and cell–matrix interactions in human models.
FKBP10 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous FKBP10 expression without altering the underlying DNA sequence.
FKBP10 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the FKBP10 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 FKBP10 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous FKBP10 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native FKBP10 locus and enabling the study of FKBP10-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of FKBP10 pathway restoration in tumor cells with silenced or reduced FKBP10 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.