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.
PKC mu CRISPR Activation Plasmid (h): sc-401070-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PKC mu CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- PKC mu 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 PKC mu CRISPR Activation Plasmid (h) and PKC mu CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the PRKD1 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: PKC mu Antibody (G-9): sc-518065
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PKC mu CRISPR Activation Plasmid (h) | sc-401070-ACT | 20 µg | $397.00 |
PRKD1 encodes protein kinase D1 (PKC mu), a serine/threonine kinase activated downstream of diacylglycerol and novel PKC signaling that coordinates phosphorylation-dependent control of membrane trafficking, cytoskeletal remodeling, and transcriptional programs. PKC mu participates in pathways linking GPCR and receptor tyrosine kinase inputs to MAPK signaling, NF-κB–associated responses, and regulation of cell survival and motility. In human cells, PRKD1 activity has been connected to modulation of epithelial polarity, secretory transport from the trans-Golgi network, and stress-responsive signaling networks. Dysregulated PRKD1 signaling has been reported across multiple disease-relevant contexts, including altered proliferative and migratory phenotypes and inflammatory signaling, supporting its use as a mechanistic node in pathway interrogation.
PKC mu CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous PRKD1 expression without altering the underlying DNA sequence.
PKC mu CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the PRKD1 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 PRKD1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous PKC mu expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native PRKD1 locus and enabling the study of PKC mu-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of PKC mu pathway restoration in tumor cells with silenced or reduced PRKD1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.