
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Asporin CRISPR Activation Plasmid (m) | sc-426152-ACT | 20 µg | $397.00 | |||
Asporin CRISPR Activation Plasmid (m2) | sc-426152-ACT-2 | 20 µg | $397.00 |
Mouse Aspn encodes asporin, a secreted small leucine-rich proteoglycan enriched in the extracellular matrix where it modulates collagen fibrillogenesis and matrix organization. Asporin regulates cell–matrix signaling and influences key pathways such as TGF-β/SMAD and BMP signaling, impacting chondrogenesis, osteogenesis, and tissue remodeling. Altered ASPN expression has been associated with connective tissue and skeletal phenotypes, including osteoarthritis-related cartilage degeneration and fibrotic remodeling contexts. These properties make Aspn a useful gene for studying extracellular matrix homeostasis, mechanotransduction, and stromal regulation of cell behavior.
Asporin CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Aspn expression without altering the underlying DNA sequence.
Asporin CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Aspn 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 Aspn transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Asporin expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Aspn locus and enabling the study of Asporin-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Asporin pathway restoration in tumor cells with silenced or reduced Aspn expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.