
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CRTAC1 CRISPR Activation Plasmid (h) | sc-404534-ACT | 20 µg | $397.00 |
CRTAC1 (cartilage acidic protein 1) encodes a secreted extracellular matrix–associated protein enriched in cartilage and other connective tissues, where it contributes to cell–matrix interactions and tissue structural organization. CRTAC1 has been linked to chondrocyte differentiation and matrix homeostasis processes that intersect with adhesion and extracellular matrix remodeling pathways. Altered CRTAC1 expression has been reported in musculoskeletal and degenerative joint conditions, making it a useful marker for studying cartilage biology and connective tissue remodeling. In vitro, CRTAC1 modulation can support mechanistic work on matrix composition, cellular adhesion phenotypes, and transcriptional programs relevant to cartilage integrity.
CRTAC1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CRTAC1 expression without altering the underlying DNA sequence.
CRTAC1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CRTAC1 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 CRTAC1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CRTAC1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CRTAC1 locus and enabling the study of CRTAC1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CRTAC1 pathway restoration in tumor cells with silenced or reduced CRTAC1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.