
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DGK-ζ CRISPR Activation Plasmid (h) | sc-403843-ACT | 20 µg | $397.00 |
Diacylglycerol kinase zeta (DGKζ), encoded by the human DGKZ gene, phosphorylates diacylglycerol (DAG) to generate phosphatidic acid, shaping the amplitude and duration of DAG-dependent signaling. By modulating second-messenger balance, DGKζ influences PKC- and Ras/ERK-linked pathways, receptor-proximal signaling, and cytoskeletal remodeling programs that affect cell activation, migration, and proliferation. DGKζ activity is also connected to phosphoinositide metabolism and signal integration downstream of immune receptors and growth factor inputs. Dysregulated DAG–phosphatidic acid signaling involving DGKζ has been implicated in studies of immune dysfunction, inflammation, and oncogenic signaling contexts, supporting its relevance as a mechanistic node in cell signaling research.
DGK-ζ CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous DGKZ expression without altering the underlying DNA sequence.
DGK-ζ CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the DGKZ 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 DGKZ transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous DGK-ζ expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native DGKZ locus and enabling the study of DGK-ζ-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of DGK-ζ pathway restoration in tumor cells with silenced or reduced DGKZ expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.