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.
Dermcidin CRISPR Activation Plasmid (h): sc-401346-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Dermcidin CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- Dermcidin 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 Dermcidin CRISPR Activation Plasmid (h) and Dermcidin CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the DCD 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: Dermcidin Antibody (H-12): sc-398429
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Dermcidin CRISPR Activation Plasmid (h) | sc-401346-ACT | 20 µg | $397.00 | |||
Dermcidin CRISPR Activation Plasmid (h2) | sc-401346-ACT-2 | 20 µg | $397.00 |
Human DCD encodes dermcidin, a secreted peptide precursor highly expressed in eccrine sweat glands that is proteolytically processed into antimicrobial and bioactive fragments. Dermcidin-derived peptides contribute to innate barrier defense by disrupting microbial membranes and shaping skin and mucosal microenvironments, while additional fragments have been linked to cellular stress responses and survival signaling. Altered DCD expression has been reported across inflammatory contexts and multiple cancer types, where it is associated with changes in proliferation, oxidative stress tolerance, and tumor–microenvironment interactions. These attributes make DCD a useful node for studying epithelial homeostasis, secreted peptide biology, and microenvironmental regulation relevant to disease-associated remodeling.
Dermcidin CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous DCD expression without altering the underlying DNA sequence.
Dermcidin CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the DCD 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 DCD transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Dermcidin expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native DCD locus and enabling the study of Dermcidin-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Dermcidin pathway restoration in tumor cells with silenced or reduced DCD expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.