
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
S-100P CRISPR Activation Plasmid (h) | sc-404366-ACT | 20 µg | $397.00 |
Human S100P encodes S-100P, a small EF-hand calcium-binding protein that functions as a signaling adaptor linking calcium flux to changes in cytoskeletal dynamics, cell-cycle control, and stress-responsive transcriptional programs. S-100P is reported to interact with receptors and signaling hubs such as RAGE, influencing MAPK and NF-κB-associated pathways that modulate adhesion, migration, and survival phenotypes. Dysregulated S100P expression has been observed across multiple epithelial malignancies and is frequently studied as a marker of tumor progression and metastatic potential. In addition, S-100P biology is relevant to inflammation-associated tissue remodeling, where calcium-dependent signaling intersects with extracellular matrix and immune cues.
S-100P CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous S100P expression without altering the underlying DNA sequence.
S-100P CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the S100P 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 S100P transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous S-100P expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native S100P locus and enabling the study of S-100P-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of S-100P pathway restoration in tumor cells with silenced or reduced S100P expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.