
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Scleraxis CRISPR Activation Plasmid (m) | sc-422833-ACT | 20 µg | $397.00 |
Mouse Scx encodes scleraxis, a basic helix–loop–helix transcription factor that functions as a lineage regulator of tendon and ligament progenitors and a key driver of extracellular matrix gene programs. Scleraxis coordinates transcriptional networks controlling tenocyte differentiation, collagen fibrillogenesis, and cytoskeletal organization in response to developmental cues and biomechanical loading, intersecting with pathways such as TGF-β/SMAD, FGF, and mechanotransduction signaling. Altered SCX expression or activity is associated with dysregulated connective tissue remodeling, impaired tendon maturation, and fibrosis-like matrix deposition, making it a useful node for studying musculoskeletal development and soft tissue repair biology.
Scleraxis CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Scx expression without altering the underlying DNA sequence.
Scleraxis CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Scx 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 Scx transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Scleraxis expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Scx locus and enabling the study of Scleraxis-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Scleraxis pathway restoration in tumor cells with silenced or reduced Scx expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.