
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Sox-7 CRISPR Activation Plasmid (m) | sc-423091-ACT | 20 µg | $397.00 |
Mouse Sox7 encodes the transcription factor Sox-7, a member of the SOX F-group that regulates endothelial differentiation, vascular morphogenesis, and maintenance of cell identity during development. Sox-7 functions in transcriptional programs that intersect with angiogenic signaling and vascular homeostasis, including crosstalk with Wnt/β-catenin and Notch-associated pathways. Altered SOX7 activity has been linked to dysregulated endothelial gene expression and aberrant vessel formation, making it relevant to studies of developmental defects and vascular-associated disease mechanisms. In addition to roles in endothelium, Sox-7 can influence epithelial–mesenchymal regulatory networks and lineage specification programs used to model tissue remodeling.
Sox-7 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Sox7 expression without altering the underlying DNA sequence.
Sox-7 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Sox7 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 Sox7 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Sox-7 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Sox7 locus and enabling the study of Sox-7-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Sox-7 pathway restoration in tumor cells with silenced or reduced Sox7 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.