
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ANKH CRISPR Activation Plasmid (m) | sc-419107-ACT | 20 µg | $397.00 | |||
ANKH CRISPR Activation Plasmid (m2) | sc-419107-ACT-2 | 20 µg | $397.00 |
Mouse Ank encodes ANKH, a multipass membrane transporter that regulates inorganic pyrophosphate (PPi) export and extracellular mineralization homeostasis. By controlling PPi availability, ANKH influences hydroxyapatite deposition, osteogenic differentiation programs, and broader phosphate/pyrophosphate metabolic balance in skeletal and joint tissues. Altered ANKH activity is linked to aberrant calcification phenotypes and joint pathology, making it a useful node for studying cartilage biology, bone remodeling, and calcification-associated inflammatory processes. This gene is frequently investigated in models of ectopic mineralization and degenerative joint disease mechanisms.
ANKH CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Ank expression without altering the underlying DNA sequence.
ANKH CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Ank 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 Ank transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ANKH expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Ank locus and enabling the study of ANKH-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ANKH pathway restoration in tumor cells with silenced or reduced Ank expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.