
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
COL10A1 CRISPR Activation Plasmid (h) | sc-401960-ACT | 20 µg | $397.00 |
COL10A1 encodes collagen type X alpha 1, a short-chain collagen expressed predominantly by hypertrophic chondrocytes during endochondral ossification. It contributes to extracellular matrix organization and cartilage-to-bone transition by shaping the pericellular matrix and supporting mineralization-associated remodeling. COL10A1 expression is tightly coupled to chondrocyte differentiation programs regulated by pathways such as TGF-β/BMP signaling, RUNX2-driven transcriptional control, and matrix turnover processes. Dysregulated COL10A1 is associated with skeletal developmental disorders including Schmid metaphyseal chondrodysplasia and is also observed in pathologic matrix remodeling contexts relevant to bone and cartilage research.
COL10A1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous COL10A1 expression without altering the underlying DNA sequence.
COL10A1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the COL10A1 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 COL10A1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous COL10A1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native COL10A1 locus and enabling the study of COL10A1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of COL10A1 pathway restoration in tumor cells with silenced or reduced COL10A1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.