
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DC-STAMP CRISPR Activation Plasmid (h) | sc-402527-ACT | 20 µg | $397.00 |
DCSTAMP encodes DC-STAMP, a multi-pass transmembrane protein essential for cell–cell fusion events that generate multinucleated osteoclasts and foreign body giant cells from monocyte/macrophage precursors. DC-STAMP integrates cues from RANKL-driven osteoclastogenesis and inflammatory signaling to coordinate differentiation and fusion, influencing bone resorption and immune microenvironment remodeling. Dysregulated DC-STAMP activity is linked to altered osteoclast function and has been studied in contexts of inflammatory bone loss, autoimmune inflammation, and tumor-associated osteoclastogenesis. As a regulator of myeloid lineage fusion and maturation, DC-STAMP is a useful handle for dissecting mechanisms of macrophage polarization, multinucleation, and osteoimmunology-relevant pathways.
DC-STAMP CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous DCSTAMP expression without altering the underlying DNA sequence.
DC-STAMP CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the DCSTAMP 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 DCSTAMP transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous DC-STAMP expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native DCSTAMP locus and enabling the study of DC-STAMP-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of DC-STAMP pathway restoration in tumor cells with silenced or reduced DCSTAMP expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.