S-100A10 CRISPR Activation Plasmid (h): sc-402230-ACT

S100A10 encodes S-100A10 (p11), a Ca2+-binding S100 family member that forms a functional heterotetramer with annexin A2 at the plasma membrane and endosomal compartments. This complex coordinates plasminogen activation and pericellular proteolysis, influencing extracellular matrix remodeling, cell adhesion, and directed migration through cytoskeletal and membrane-trafficking processes. S-100A10 also participates in inflammatory signaling and stress-response pathways by modulating receptor localization and protease networks at the cell surface. Dysregulated S100A10 expression has been reported across multiple disease contexts, including cancer-associated invasion and metastasis, vascular and fibrotic remodeling, and neuroinflammatory phenotypes, supporting its utility as a mechanistic target in pathway-focused research.

S-100A10 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous S100A10 expression without altering the underlying DNA sequence.

S-100A10 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the S100A10 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 S100A10 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous S-100A10 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native S100A10 locus and enabling the study of S-100A10-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of S-100A10 pathway restoration in tumor cells with silenced or reduced S100A10 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.