
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
COL12A1 CRISPR Activation Plasmid (h) | sc-402361-ACT | 20 µg | $397.00 |
COL12A1 encodes collagen type XII alpha 1 chain, a fibril-associated collagen with interrupted triple helices (FACIT) that localizes to the extracellular matrix and binds collagen I–containing fibrils to regulate fibrillogenesis, matrix organization, and tissue mechanical properties. It is enriched in connective tissues and contributes to cell–matrix adhesion, mechanotransduction, and coordinated remodeling during development and repair. Altered COL12A1 expression or function is linked to heritable connective tissue disorders featuring musculoskeletal phenotypes, reflecting its role in tendon/ligament integrity and cartilage-bone interfaces. In cancer biology and fibrotic remodeling, COL12A1 is frequently studied as a stromal ECM component associated with matrix stiffness and invasive microenvironments.
COL12A1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous COL12A1 expression without altering the underlying DNA sequence.
COL12A1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the COL12A1 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 COL12A1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous COL12A1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native COL12A1 locus and enabling the study of COL12A1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of COL12A1 pathway restoration in tumor cells with silenced or reduced COL12A1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.