Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Periostin CRISPR Activation Plasmid (h): sc-400744-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Periostin CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- Periostin CRISPR Activation Plasmid (h) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by Periostin CRISPR Activation Plasmid (h) and Periostin CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the POSTN transcriptional start site. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Periostin Antibody (F-10): sc-398631
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Periostin CRISPR Activation Plasmid (h) | sc-400744-ACT | 20 µg | $397.00 | |||
Periostin CRISPR Activation Plasmid (h2) | sc-400744-ACT-2 | 20 µg | $397.00 |
POSTN encodes periostin, a secreted matricellular protein enriched in connective tissues that binds extracellular matrix components and integrins to regulate cell adhesion, migration, and tissue remodeling. Periostin participates in extracellular matrix organization and mechanotransduction, supporting signaling through focal adhesion and downstream pathways such as FAK/PI3K/AKT and MAPK that influence fibroblast activation and epithelial–mesenchymal interactions. Altered POSTN expression is associated with fibrotic remodeling and inflammatory tissue responses, and it is frequently linked to tumor microenvironment dynamics including stromal expansion, angiogenic cues, and metastatic niche formation. These properties make periostin a useful molecular handle for studying extracellular matrix–driven signaling and cell–matrix crosstalk across disease-relevant models.
Periostin CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous POSTN expression without altering the underlying DNA sequence.
Periostin CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the POSTN 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 POSTN transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Periostin expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native POSTN locus and enabling the study of Periostin-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Periostin pathway restoration in tumor cells with silenced or reduced POSTN expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.