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.
PKD2 CRISPR Activation Plasmid (m): sc-430381-ACT
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PKD2 CRISPR Activation Plasmid (m) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- PKD2 CRISPR Activation Plasmid (m) 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 PKD2 CRISPR Activation Plasmid (m) and PKD2 CRISPR Activation Plasmid (m2) target distinct regulatory regions upstream of the Prkd2 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: PKD2 Antibody (F-2): sc-374344
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PKD2 CRISPR Activation Plasmid (m) | sc-430381-ACT | 20 µg | $397.00 | |||
PKD2 CRISPR Activation Plasmid (m2) | sc-430381-ACT-2 | 20 µg | $397.00 |
Prkd2 encodes protein kinase D2 (PKD2), a serine/threonine kinase in the CAMK-like PKD family that transduces signals downstream of diacylglycerol and protein kinase C. PKD2 regulates phosphorylation-dependent control of gene expression, vesicle trafficking from the trans-Golgi network, cytoskeletal remodeling, and stress-responsive survival programs, integrating inputs from GPCR and receptor tyrosine kinase signaling. In mouse cells, PKD2 activity has been linked to pathways governing immune cell activation, inflammatory signaling, and cell migration through modulation of MAPK- and NF-κB-associated transcriptional outputs. Dysregulated PKD2 signaling is studied in contexts such as aberrant proliferation, tissue remodeling, and inflammatory disease mechanisms, supporting its utility as a node for pathway interrogation.
PKD2 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Prkd2 expression without altering the underlying DNA sequence.
PKD2 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Prkd2 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 Prkd2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous PKD2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Prkd2 locus and enabling the study of PKD2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of PKD2 pathway restoration in tumor cells with silenced or reduced Prkd2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.